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Secondary caries is one of the main reasons for dental filling replacement. There is a need to obtain dental restorative material that is able to act against caries-inducing microorganisms. This study explores the antimicrobial properties of cetyltrimethylammonium bromide (CTAB) or dimethyldioctadecylammonium bromide (DODAB)-modified photo-cured experimental dental composites against Escherichia coli, Streptococcus mutans, and Candida albicans. The antimicrobial activity against Escherichia coli, Streptococcus mutans, and Candida albicans was assessed by using an Accuri C6 flow cytofluorimeter, and then analyzed using BD CSampler software (1.0.264). Bacterial/yeast surface colonization was carried out by using an GX71 inverted-optics fluorescence microscope equipped with a DP 73 digital camera. For bactericidal surface analysis of each sample type, simultaneous standardization was performed using a positive control (live cells) and a negative control (dead cells). A positive correlation between the increasing concentration of CTAB or DODAB and the dead cell ratio of Escherichia coli, Streptococcus mutans, and Candida albicans was revealed. In particular, CTAB at a 2.0 wt% concentration exhibits superior efficiency against pathogens (65.0% dead cells of Escherichia coli, 73.9% dead cells of Streptococcus mutans, and 23.9% dead cells of Candida albicans after 60 min). However, Candida albicans is more resistant to used salts than bacteria. A CTAB- or DODAB-modified experimental dental composite exhibits antimicrobial potential against Escherichia coli, Streptococcus mutans, and Candida albicans after 10 and 60 min of incubation, and the antimicrobial efficiency increases with the wt% of QAS in the tested material. [ABSTRACT FROM AUTHOR]

Yeasts derived from fermented foods have historically been known for their organoleptic properties, enriching nutritional values, and producing bioactive metabolites with therapeutic potential. In this review, we discuss the yeast flora in fermented foods, their functional aspects in fermentation, as well as their probiotic and biotherapeutic properties. These yeasts have numerous physical and biochemical characteristics, such as larger cells as compared to bacteria, a rigid cell wall composed primarily of glucans and mannans, natural resistance to antibiotics, and the secretion of secondary metabolites that are both pleasing to the consumer and beneficial to the host's health and well-being. The review also focused on therapeutic applications of probiotic yeasts derived from fermented foods on infections associated with Candida species. These potential probiotic yeasts present an additional avenue to treat dysbiosis of the gut microbiota and prevent health complications that arise from opportunistic fungal colonization, especially drug-resistant superbugs, which are highlighted in this review. [ABSTRACT FROM AUTHOR]

Vulvovaginal candidiasis (VVC) is a genital infection caused by Candida albicans (C. albicans). Weissella confusa WIKIM51 (Wilac D001) is known to be detected in dandelion kimchi, produce lactic acid, and have an anti−inflammatory ability; however, its diverse antifungal effects have not been studied. Here, we investigated the antifungal effect of Wilac D001 in C. albicans compared to Lactobacillus species on vaginal epithelial cells (VECs). To test the antifungal ability of Wilac D001 against C. albicans on VECs, an adhesion test, pro-inflammatory cytokines (interleukin (IL)-6 and IL-8) analysis, and a disk diffusion test were performed. The acid tolerance test was conducted to investigate the viability of Wilac D001 in various acidic conditions. Lactobacillus reuteri (L. reuteri) and L. rhamnosus were used as positive controls. Wilac D001 showed the capacity to inhibit the colonization of C. albicans by adhering to VECs, with an inhibitory effect similar to that of positive controls. Both pro−inflammatory cytokines including IL−6 and IL−8 concentrations were significantly decreased when Wilac D001 was treated on C. albicans-infected VECs, respectively (p < 0.001). The result of the disk diffusion test indicates that the inhibitory ability of Wilac D001 is comparable to L. reuteri and L. rhamnosus on agar plates infected with C. albicans. Our results demonstrate that Weissella confusa WIKIM51 has antifungal effects against VECs infected by C. albicans. [ABSTRACT FROM AUTHOR]

Candida albicans is a commensal yeast that has important impacts on host metabolism and immune function, and can establish life-threatening infections in immunocompromised individuals. Previously, C. albicans colonization has been shown to contribute to the progression and severity of alcoholic liver disease. However, relatively little is known about how C. albicans responds to changing environmental conditions in the GI tract of individuals with alcohol use disorder, namely repeated exposure to ethanol. In this study, we repeatedly exposed C. albicans to high concentrations (10% vol/vol) of ethanol—a concentration that can be observed in the upper GI tract of humans following consumption of alcohol. Following this repeated exposure protocol, ethanol small colony (Esc) variants of C. albicans isolated from these populations exhibited increased ethanol tolerance, altered transcriptional responses to ethanol, and cross-resistance/tolerance to the frontline antifungal fluconazole. These Esc strains exhibited chromosomal copy number variations and carried polymorphisms in genes previously associated with the acquisition of fluconazole resistance during human infection. This study identifies a selective pressure that can result in evolution of fluconazole tolerance and resistance without previous exposure to the drug. [ABSTRACT FROM AUTHOR]

Despite being common, the pathogenesis of denture stomatitis (DS) is poorly known; thus, this study was conducted to examine the relationship between candida, dentures, and mucosal tissue inflammation. One hundred and twenty edentulous patients wearing a denture with clinical signs and symptoms of DS and 30 patients without DS as healthy were involved in the study. Patients with DS were divided into three groups according to Newton's classification and fungal colonies, and denture fit was assessed. No significant difference was observed between age, sex, and denture fit between the two groups (P > 0.05). The fungal colonies in patients with DS were significantly more than the controls. The majority of the patients with good denture fit had degree 1 (localized mucosal inflammation), while the majority of the patients with fair denture fit had degree 2 (diffuse inflammation on the denture bearing area) and the majority with poor denture fit had degree 3 (granular type) (P < 0.001). The fungal colonies were negative for the majority of degree 1 patients (57.1%), while they were positive for the majority of patients with degree 2 (61.3%) and degree 3 (63.2%) inflammation (P = 0.003). We concluded that the pathogenesis of DS is elusive. Multiple factors, including lack of hygiene, reduced salivary flow, poor denture care, and fit, provide an easy pathway for Candida strains to colonize dentures. [ABSTRACT FROM AUTHOR]

Candida albicans is a pathogenic fungus recently recognized for its role in severe early childhood caries development (S-ECC). C. albicans oral colonization begins at birth, but the extent of the mother's involvement in yeast transmission to their children is unclear, therefore, this study used a prospective mother-infant cohort to investigate the maternal contribution of C. albicans oral colonization in early life. Oral samples were collected from 160 mother-child dyads during pregnancy and from birth to two years of life. We used whole-genome sequencing to obtain the genetic information of C. albicans isolates and examined the genetic relatedness of C. albicans between mothers and their children using Multilocus Sequence Typing. Multivariate statistical methods were used to identify factors associated with C. albicans' acquisition (horizontal and vertical transmissions). Overall, 227 C. albicans oral isolates were obtained from 93 (58.1%) of mother-child pairs. eBURST analysis revealed 16 clonal complexes, and UPGMA analysis identified 6 clades, with clade 1 being the most populated 124 isolates (54.6%). Significantly, 94% of mothers and children with oral C. albicans had highly genetically related strains, highlighting a strong maternal influence on children's C. albicans acquisition. Although factors such as race, ethnicity, delivery method, and feeding behaviors did not show a significant association with C. albicans vertical transmission, the mother's oral hygiene status reflected by plaque index (PI) emerged as a significant factor; Mothers with higher dental plaque accumulation (PI >=2) had a significantly increased risk of vertically transmitting C. albicans to their infants [odds ratio (95% confidence interval) of 8.02 (1.21, 53.24), p=0.03]. Furthermore, Black infants and those who attended daycare had an elevated risk of acquiring C. albicans through horizontal transmission (p <0.01). These findings highlight the substantial role of maternal transmission in the oral acquisition of C. albicans during early life. Incorporating screening for maternal fungal oral carriage and implementing oral health education programs during the perinatal stage may prove valuable in preventing fungal transmission in early infancy. [ABSTRACT FROM AUTHOR]

To investigate the effect of various concentrations of chitosan oligosaccharide solution (COS) and different immersion times on the antifungal activity against Candida albicans (C. albicans) on heat-cured polymethylmethacrylate (PMMA) and examine the color stability after 28 days of application. The specimens were immersed in distilled water (DW), 0.2% Chlorhexidine gluconate (CHX) and various concentrations of COS. A number of fungal colonies were recorded after 1 and 8 h of immersion. The most effective method was further examined for color stability using a colorimeter and the Commission Internationale de I'Eclairage (CIE) L*a*b* system. The color alterations were determined at day 0, 1, 7, 14, 21, and 28 of immersion. Data were analyzed using Two-way ANOVA (p<0.05). The efficiency in reducing the viability of C. albicans biofilm was better in COS than DW but lower than CHX. There was no significant difference among various COS concentrations. 8-h immersion showed greater inhibition compared to 1 h. Moreover, the color of all specimens changed significantly within clinically acceptable limits after 28 days of immersion. The greatest discoloration was found with CHX. Immersing dentures in 0.5 MFC (350 mg/ml) COS for 8 h can effectively reduce C. albicans viability without compromising the color stability of heat-cured PMMA. [ABSTRACT FROM AUTHOR]

Candida albicans is an opportunistic fungal pathogen that can cause superficial and invasive infections. Seventy-five percent of women suffer from vaginal candidiasis at least once in their lifetime, 372 million women are currently suffering from recurrent vulvovaginal candidiasis, and 700 000 cases of invasive candidiasis are reported yearly, with an associated mortality of 30–40%. Bacteria from the gut and vaginal microbiota can control C. albicans growth by the release of antifungal metabolites, modulation of the host immune response, and/or competition for nutrients, niches, and adhesion sites. Cutting-edge OMICs-based pipelines, relying on metagenomics and/or metabolomics, have permitted the identification of bacterial species and metabolites with potential antifungal activities. The development of experimental platforms has allowed the validation and screening of new anti- C. albicans bacteria. In silico and experimental approaches have allowed an ever-growing understanding of the interactions within the microbiota. For instance, recently acquired data have increased knowledge of the mechanisms that support, in the gut and vaginal microbiota, the resistance to colonization by Candida albicans , an opportunistic fungal pathogen whose overgrowth can initiate severe infections in immunocompromised patients. Here, we review how bacteria from the microbiota interact with C. albicans. We show how recent OMICs-based pipelines, using metagenomics and/or metabolomics, have identified bacterial species and metabolites modulating C. albicans growth. We finally discuss how the combined use of cutting-edge OMICs-based and experimental approaches could provide new means to control C. albicans overgrowth within the microbiota and prevent its consequences. [ABSTRACT FROM AUTHOR]

Candida albicans commensalism and pathogenesis is influenced by microbial communities through cross-kingdom interactions. Disruption of mucosal barriers and bacterial communities by antibiotic treatment or inflammatory disease can initiate or enhance C. albicans pathogenesis. C. albicans gastrointestinal colonization is critical for shaping host immune responses to infection. Antagonistic and synergistic Candida– bacteria interactions affect fungal and bacterial virulence. Ongoing study of Candida– bacteria interactions may reveal novel antifungal compounds for treating invasive disease. While the fungus Candida albicans is a common colonizer of healthy humans, it is also responsible for mucosal infections and severe invasive disease. Understanding the mechanisms that allow C. albicans to exist as both a benign commensal and as an invasive pathogen have been the focus of numerous studies, and recent findings indicate an important role for cross-kingdom interactions on C. albicans biology. This review highlights how C. albicans– bacteria interactions influence healthy polymicrobial community structure, host immune responses, microbial pathogenesis, and how dysbiosis may lead to C. albicans infection. Finally, we discuss how cross-kingdom interactions represent an opportunity to identify new antivirulence compounds that target fungal infections. [ABSTRACT FROM AUTHOR]

Candida albicans filamentation plays a significant role in developing both mucosal and invasive candidiasis, making it a crucial virulence factor. Consequently, exploring and identifying inhibitors that impede fungal hyphal formation presents an intriguing approach toward antifungal strategies. In line with this anti-filamentation strategy, we conducted a comprehensive screening of a library of FDA-approved drugs to identify compounds that possess inhibitory properties against hyphal growth. The compound octenidine dihydrochloride (OCT) exhibits potent inhibition of hyphal growth in C. albicans across different hyphae-inducing media at concentrations below or equal to 3.125 μM. This remarkable inhibitory effect extends to biofilm formation and the disruption of mature biofilm. The mechanism underlying OCT's inhibition of hyphal growth is likely attributed to its capacity to impede ergosterol biosynthesis and induce the generation of reactive oxygen species (ROS), compromising the integrity of the cell membrane. Furthermore, it has been observed that OCT demonstrates protective attributes against invasive candidiasis in Galleria mellonella larvae through its proficient eradication of C. albicans colonization in infected G. mellonella larvae by impeding hyphal formation. Although additional investigation is required to mitigate the toxicity of OCT in mammals, it possesses considerable promise as a potent filamentation inhibitor against invasive candidiasis. [ABSTRACT FROM AUTHOR]

In the present work, a series of N-terpenyl organoselenium compounds (CHB1-6) were evaluated for antimycotic activity by determining the minimum inhibitory concentration (MIC) for each compound in fluconazole (FLU)-sensitive (S1) and FLU-resistant (S2) strains of Candida albicans (C. albicans). The most active compounds in the MIC screen were CHB4 and CHB6, which were then evaluated for cytotoxicity in human cervical cancer cells (KB-3-1) and found to be selective for fungi. Next, CHB4 and CHB6 were investigated for skin irritation using a reconstructed 3D human epidermis and both compounds were considered safe to the epidermis. Using a mouse model of vulvovaginal candidiasis (VVC), CHB4 and CHB6 both exhibited antimycotic efficacy by reducing yeast colonization of the vaginal tract, alleviating injury to the vaginal mucosa, and decreasing the abundance of myeloperoxidase (MPO) expression in the tissue, indicating a reduced inflammatory response. In conclusion, CHB4 and CHB6 demonstrate antifungal activity in vitro and in the mouse model of VVC and represent two new promising antifungal agents. [ABSTRACT FROM AUTHOR]

This study evaluated surface properties and adhesion/biofilm formation by Candida albicans on 3D printed denture base resins used in 3D printing. Disc-shaped specimens (15 mm x 3 mm) of two 3D-printed resins (NextDent Denture 3D+, NE, n = 64; and Cosmos Denture, CO, n = 64) and a heat-polymerized resin (Lucitone 550, LU, control, n = 64) were analyzed for surface roughness (Ra μm) and surface free energy (erg cm-2). Microbiologic assays (90-min adhesion and 48-h biofilm formation by C. albicans) were performed five times in triplicate, with the evaluation of the specimens' surface for: (i) colony forming units count (CFU/mL), (ii) cellular metabolism (XTT assay), and (iii) fluorescence and thickness of biofilm layers (confocal laser scanning microscopy). Data were analyzed using parametric and nonparametric tests (α = 0.05). LU presented higher surface roughness Ra (0.329±0.076 μm) than NE (0.295±0.056 μm) (p = 0.024), but both were similar to CO (0.315±0.058 μm) (p = 1.000 and p = 0.129, respectively). LU showed lower surface free energy (47.47±2.01 erg cm-2) than CO (49.61±1.88 erg cm-2) and NE (49.23±2.16 erg cm-2) (p<0.001 for both). The CO and NE resins showed greater cellular metabolism (p<0.001) and CO only, showed greater colonization (p = 0.015) by C. albicans than LU in the 90-min and 48-hour periods. It can be concluded that both 3D-printed denture base resins are more prone to colonization by C. albicans, and that their surface free energy may be more likely associated with that colonization than their surface roughness. [ABSTRACT FROM AUTHOR]

Introduction: The peri‐implant sulcus is a good niche for infectious colonization such as Candida spp. In this study, the level of Candida spp. fungal colonization is analyzed in patients with peri‐implantitis under supportive peri‐implant therapy, as well as its correlation with the main clinicopathological data. Methods: A case–control study was carried out on 161 patients treated with dental implants, 80 with PI and 81 without PI, which corresponded to 91 women and 70 men, whose mean age was 60.90 years. A specific protocol was completed for the clinical and implant data. Microbiological samples were taken by oral rinse and with paper tips from the peri‐implant sulcus. For the quantitative and qualitative analysis Candida Chromogenic Agar/CONDA plates were incubated for 72 h at 36 + 1°C. Fungal growth was considered active when having more than 50 CFU. Specific Candida spp. cultures were later confirmed by API ID 32C and PCR. Results: Fungal growth was achieved in 28% of oral rinse and 6.75% of peri‐implant fluid samples. No significant differences were recognized between study groups. Most of the cultures (>65%) showed more than 50 CFU. The most frequent species were Candida albicans and Candida parapsilosis. There was no association between different PI risk factors and fungal data. The presence of Candida spp. in the oral cavity of patients with dental implants was related to total edentulism and the use of implant‐fixed complete prosthesis implant‐retained removable prosthesis. Conclusions: These results suggest that there is no link between PI and presence of Candida in patients with dental implants undergoing regular supportive periodontal therapy. [ABSTRACT FROM AUTHOR]

Copyright of Current Research in Dental Sciences is the property of Ataturk University Coordinatorship of Scientific Journals and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

The development of efficient fungal vaccines is urgent for preventing life-threatening systemic fungal infections. In this study, we prepared a synthetic, cell-based fungal vaccine for preventing systemic fungal infections using synthetic biology techniques. The synthetic cell EmEAP1 was constructed by transforming the Escherichia coli chassis using a de novo synthetic fragment encoding the protein mChEap1 that was composed of the E. coli OmpA peptide, the fluorescence protein mCherry, the Candida albicans adhesin Eap1, and the C-terminally transmembrane region. The EmEAP1 cells highly exposed the mChEap1 on the cell surface under IPTG induction. The fungal vaccine was then prepared by mixing the EmEAP1 cells with aluminum hydroxide gel and CpG. Fluorescence quantification revealed that the fungal vaccine was stable even after 112 days of storage. After immunization in mice, the vaccine resided in the lymph nodes, inducing the recruitment of CD11c+ dendritic cells. Moreover, the vaccine strongly activated the CD4+ T splenocytes and elicited high levels of anti-Eap1 IgG. By the prime-boost immunization, the vaccine prolonged the survival time of the mice infected by the C. albicans cells and attenuated fungal colonization together with inflammation in the kidneys. This study sheds light on the development of synthetic biology-based fungal vaccines for the prevention of life-threatening fungal infections. [ABSTRACT FROM AUTHOR]

C. albicans colonization affects the gut-brain axis Impacts of the gut microbiota on the brain through the gut-brain axis have recently become the subject of investigation. The gut-brain axis is defined as the bidirectional communication between the brain and the gastrointestinal tract through direct and indirect pathways including direct neuronal innervation of the intestines, metabolic pathways, and immune system modulation. I albicans i colonization changed the gut metabolite environment in a way that reduced I C i . I albicans i is not the only organism to affect susceptibility to bacterial infection or signaling in the gut-brain axis. [Extracted from the article]

Backgrounds: A proper disinfection of denture is vital to prevent a fungal infection. A study on the feasibility of microencapsulated phytochemical as complementary disinfectant and its interaction with effervescent tablet immersion on denture base resin is lacking. Objectives: The aim of this study was to examine the feasibility of phytochemical-filled microcapsules as disinfectant for the inhibition of Candida albicans (C. albicans) attachment on the denture base produced by digital light processing (DLP). Methods: 54 denture base specimens uniformly mixed with or without 5wt% phytochemical-filled microcapsules were prepared using DLP. Fungal cells were inoculated onto the surfaces of the specimens, which were divided into three different disinfection treatment groups (n = 9): 1) none, 2) sterile tap water immersion for 15 min, and 3) effervescent tablet immersion for 15 min. After each treatment, the biofilm on denture surface was stained with a crystal violet solution to measure the absorbance. The number of fungal colonies was counted as colony-forming units (CFU) per mL. Morphological changes were examined by microscopy. An aligned rank transform analysis of variance was performed to analyze the interaction of presence of microcapsule and disinfection condition, with statistical significance set at P < 0.05. Results: Both for the absorbance and CFU, there was no significant interaction between the presence of microcapsules and disinfection conditions (P = 0.543 and P = 0.077, respectively). The presence of microcapsules was statistically significant (both P < 0.001), while the effect of disinfection condition was not significant (P = 0.165 and P = 0.189, respectively). Morphological changes in fungi were detected in the groups containing microcapsules, whereas undamaged hyphal structures were found in those without microcapsules, irrespective of disinfection treatments. Conclusions: The presence of phytochemical-filled microcapsules significantly reduced the adhesion of C. albicans and inhibited its proliferation on denture surfaces, regardless of disinfection conditions. [ABSTRACT FROM AUTHOR]

Aim: Soft denture lining materials are susceptible to be colonized by different microorganisms, especially by Candida albicans (C. albicans), causing denture-induced stomatitis. This study was designed to evaluate the effectiveness of incorporating titanium dioxide nanoparticles (TiO2 NPs) into a soft denture liner towards reducing microbial activity. Method: A total of 40 PEMA-TiO2 nanocomposites samples were fabricated by adding 0.0 wt.% (control), 1.0 wt.%, 1.5 wt.%, and 2 wt.% TiO2 NPs to a heat cured soft denture lining material (polyethyl methacrylate, PEMA). The prepared samples were divided into four groups (n = 10) according to the content of TiO2 NPs. The uniformity of TiO2 NPS distribution within the denture liner matrix was assessed using a Scanning Electron Microscope (SEM). The viable count of C. albicans was evaluated to test the antifungal resistance of the developed composite. Results: The SEM images showed fairly homogeneous dispersion, with patches of TiO2 NPs agglomeration within the PEMA matrix and an increasing concentration of NPs with higher NP content. The particle map and EDX analysis confirmed the evidence of the TiO2 NPs. The mean viable count results for the control (0.0 wt.%) and 1.0 wt.%, 1.5 wt.%, and 2 wt.% TiO2 groups were 139.80, 12.00, 6.20, and 1.00, respectively, with a significant difference from the control group (p < 0.05). The antifungal activity also increased with the increase in the concentration of TiO2 NPs. Conclusions: The addition of TiO2 NPs into a heat-cured soft denture liner provided antifungal activity as evidenced by the reduced colonization of C. albicans. The antimicrobial activity of the liner material increased with the increased concentration of TiO2 NPS. [ABSTRACT FROM AUTHOR]

Objective: Gut mycobiota plays a crucial role in benign liver diseases; however, its correlation with hepatocellular carcinoma (HCC) remains elusive. This study aimed to elucidate fungal differences in patients with HCC-associated cirrhosis compared to cirrhotic patients without HCC and healthy controls. Methods: The 72 fecal samples from 34 HCC patients, 20 cirrhotic patients, and 18 healthy controls were collected and analyzed using ITS2 rDNA sequencing. Results: Our results revealed the presence of intestinal fungal dysbiosis with significant enrichment of opportunistic pathogenic fungi such as Malassezia, Malassezia sp., Candida, and C. albicans in HCC patients compared with healthy controls and cirrhosis patients. Alpha-diversity analysis demonstrated that patients with HCC and cirrhosis showed decreased fungal diversity compared to healthy controls. Beta diversity analysis indicated that the three groups exhibited significant segregated clustering. Besides, C. albicans was found to be significantly more abundant in the HCC patients with TNM stage III-IV than those with stage I-II, in contrast to the commensal organism S. cerevisiae. We also confirmed that the HCC patients were successfully classified with an area under the curve value of 0.906 based on the fecal fungal signature. Finally, our animal experiments confirm that aberrant colonization of the intestine by C. albicans and M. furfur can promote the development of HCC. Conclusions: This study indicates that dysbiosis of the gut mycobiome might be involved in HCC development. Trial registration: ChiCTR, ChiCTR2100054537. Registered 19 December 2021, http://www.chictr.org.cn/edit.aspx?pid=144550&htm=4 [ABSTRACT FROM AUTHOR]

White spot lesions (WSLs) are common enamel infectious diseases in fixed orthodontic treatment, which might attribute to the dysbiosis of oral microbiome. However, the correlation of Candida albicans with oral bacteriome in WSLs still remains unrevealed. This study investigated the carriage of C. albicans and how it shaped the bacterial community in disease or healthy supragingival plaque, to explore the potential role of interkingdom interaction in orthodontic WSLs. In this study, 31 patients with WSLs (WSLs) and 23 healthy patients (Health) undergoing fixed orthodontic treatment were enrolled. The supragingival microbiota in both groups were determined using 16S rRNA gene sequencing. Colonization and abundance of C. albicans in the plaque were determined via culture-dependent and -independent methods. Among WSLs patients, the correlation of C. albicans and bacteriome was analyzed under QIIME2-based bioinformatics and Spearman's correlation coefficient. The raw reads were deposited into the NCBI Sequence Read Archive (SRA) database (Accession Number: SRP404186). Significant differences in microbial diversity as well as composition were observed between WSLs and Health groups. Leptotrichia remarkably enriched in the WSLs group, while Neisseria and Cardiobacterium significantly enriched in the Health group. In addition, 45% of WSLs patients were C. albicans carriers but none in patients without WSLs. Among all WSLs patients, beta diversity and microbial composition were distinguished between C. albicans carriers and non-carriers. In C. albicans carriers, Corynebacterium matruchotii and Streptococcus mutans significantly enriched whereas Saccharibacteria_TM7_G-1 significantly depleted. The abundance of C. albicans was positively associated with bacteria such as Streptococcus mutans, while the negative correlation was detected between C. albicans and several bacteria such as Cardiobacterium hominis and Streptococcus sanguinis. Our study elucidated the distinguished supragingival plaque microbiome between orthodontic patients with and without WSLs. C. albicans frequently existed and enriched in orthodontic derived WSLs. The carriage of C. albicans shape plaque bacterial community in demineralized lesions and might play roles in WSLs pathogenesis. [ABSTRACT FROM AUTHOR]

Invasive candidiasis is an important cause of morbidity and mortality, and its occurrence is increasing due to the growing complexity of patients. In particular, Candida albicans exhibits several virulence factors that facilitate yeast colonization in humans. In this sense, the photodynamic inactivation of yeasts is a promising new alternative to eliminate fungal infections. Herein, the photodynamic activity sensitized by a free-base chlorin (TPCF16) and its complexes with Zn(II) (ZnTPCF16) and Pd(II) (PdTPCF16) was investigated in order to eliminate C. albicans under different forms of cell cultures. A decrease in cell survival of more than 5 log was found in planktonic cells incubated with 5 μM TPCF16 or ZnTPCF16 upon 15 min of white-light irradiation. The mechanism of action mainly involved a type II pathway in the inactivation of C. albicans cells. In addition, the photodynamic action induced by these chlorins was able to suppress the growth of C. albicans in a culture medium. These photosensitizers were also effective to photoinactivate C. albicans pseudohyphae suspended in PBS. Furthermore, the biofilms of C. albicans that incorporated the chlorins during the proliferation stage were completely eradicated using 5 μM TPCF16 or ZnTPCF16 after 60 min of light irradiation. The studies indicated that these chlorins are effective photosensitizing agents to eliminate C. albicans as planktonic cells, pseudohyphae, and biofilms. [ABSTRACT FROM AUTHOR]

Candida albicans is a commensal yeast that inhabits the gastrointestinal tract of humans; increased colonization of this yeast in this niche has implicated the master regulator of the white-opaque transition, Wor1, by mechanisms not completely understood. We have addressed the role that this transcription factor has on commensalism by the characterization of strains overexpressing this gene. We show that WOR1 overexpression causes an alteration of the total lipid content of the fungal cell and significantly alters the composition of structural and reserve molecular species lipids as determined by lipidomic analysis. These cells are hypersensitive to membrane-disturbing agents such as SDS, have increased tolerance to azoles, an augmented number of peroxisomes, and increased phospholipase activity. WOR1 overexpression also decreases mitochondrial activity and results in altered susceptibility to certain oxidants. All together, these changes reflect drastic alterations in the cellular physiology that facilitate adaptation to the gastrointestinal tract environment. [ABSTRACT FROM AUTHOR]

• The fungal load in tissues increases depending on host immunity. • The elevated levels of the antibodies production (IgA and IgG) and immunological markers (IL-17, and TLR2) in serum and the gut. Candida species are a normal human flora in humans' digestive and reproductive systems, oral cavity, skin, and mucosal surfaces. This study aimed to detect the immunological role of Candida infection by using some immunological markers. The results of levels in serum showed high concentrations of IgA (56.20 ± 12 pg/ml,29.55 ± 4.5 pg/ml respectively) and IgG (12.05 ± 3.218 pg/ml, 3.836 ± 1.23 pg/ml respectively) in mice infected with C. albicans and mice treated with Cefoperazone and infected with Candida with significant differences (P value < 0.05). The results showed high serum levels of IL-17(191.5 ± 42.81 pg/ml) and TLR2(7.651 ± 1.5 pg/ml) in group mice infected with C. albicans compared with negative control and group mice treated with Cefoperazone. Also, high levels of IL-17 (91.33 ± 4.816 pg/ml) and TLR2 (2.630 ± 0.5 pg/ml) in group mice treated with Cefoperazone and infected with Candida compared with negative control and group mice treated with Cefoperazone (P value < 0.05). The results of antibodies and immunological markers in the intestine showed high levels of IgA and IgG in mice infected with C.albicans (55.7 ± 4.9 pg/ml, 18.19 ± 0.63 pg/ml respectively).Also,IgA and IgG in mice treated with Cefoperazone and infected with Candida were high level (43.04 ± 2.1 pg/ml, 2.927 ± 0.2 pg/ml respectively) in mice infected with C. albicans with significant differences (P value < 0.05). The results levels of IL-17 and TLR2 were increased in mice infected with C. albicans (191.5 ± 42.81 pg/ml, 7.651 ± 1.5 pg/ml respectively) and mice treated with Cefoperazone and infected with Candida (91.33 ± 4.816 pg/ml,2.630 ± 0.5 pg/ml respectively) with significant differences (P < 0.05). In conclusion, this study demonstrated that cefoperazone treatment and infection by Candida albicans changed the microbiome components in the gut and finally can change host immune responses. It was observed that elevated levels of the antibodies production (IgA and IgG) and immunological markers (IL-17, and TLR2) in serum and the gut. [ABSTRACT FROM AUTHOR]

Candida albicans is an opportunistic pathogenic fungus, which tends to infect the host with defective immune function including cancer patients. A growing number of studies have shown that C. albicans infection increases the host susceptibility to cancer such as oral, gastric, and colorectal cancer. Cancer and anti-cancer treatment may also affect the colonization of C. albicans. C. albicans may promote the development of cancer by damaging mucosal epithelium, inducing the production of carcinogens, triggering chronic inflammation including Th17 cell-mediated immune response. In this article, we aim to elaborate the interaction between C. albicans and cancers development and summarize the potential molecular mechanisms, so as to provide theoretical basis for prevention, diagnosis and treatment of cancers. [ABSTRACT FROM AUTHOR]

Mucosal tissues are constitutively colonized by a wide assortment of host-adapted microbes. This includes the polymorphic fungus Candida albicans which is a primary target of human adaptive responses. Immunogenicity is replicated after intestinal colonization in preclinical models with a surprising array of protective benefits for most hosts, but harmful consequences for a few. The interaction between fungus and host is complex, and traditionally, the masking of antigenic fungal ligands has been viewed as a tactic for fungal immune evasion during invasive infection. However, we propose that dynamic expression of cell wall moieties, host cell lysins, and other antigenic C. albicans determinants is necessary during the more ubiquitous context of intestinal colonization to prime immunogenicity and optimize mammalian host symbiosis. Fungi including Candida albicans colonize the human intestine with local and systemic host benefits, which require fungal immunogenicity in the commensal state. Investigating the molecular and cellular mechanisms sustaining this immunological symbiosis can generate approaches to therapeutically fine-tune immunity, optimize host protection, yet limit invasion. Fungi that colonize the intestine convey unique symbiotic host benefits including tonic calibration of systemic immunity, and protection against invasive infection in rodents with potentially direct translational relevance to human immunity. Candida albicans colonization in mice protects against infection by antigenically unrelated pathogens, aberrant intestinal inflammation and injury, and can promote social behavior changes through systemic immunological influence. Immunogenicity during commensal colonization is beneficial to mice and occurs with dynamically regulated exposure of antigenic fungal cell wall ligands. Commensal C. albicans in mice are mucosa associated and can protect against intestinal injury induced by other commensal fungal species that primarily reside in the intestinal lumen. Commensal C. albicans are heterogeneous in humans and mice, with variations in immune-cell-damaging capacity associated with filamentation and production of the toxin candidalysin. [ABSTRACT FROM AUTHOR]

Abstract IL-17 plays important roles in host defense against Candida albicans at barrier surfaces and during invasive infection. However, the role of IL-17 in host defense after colonization of the epidermis, a main site of C. albicans infection, remains poorly understood. Using a murine model of epicutaneous candidiasis without skin abrasion, we found that skin inflammation triggered by epidermal C. albicans colonization was self-limiting with fungal clearance completed by day 7 after inoculation in wild-type mice or animals deficient in IL-17A or IL-17F. In contrast, marked neutrophilic inflammation in the epidermis and impaired fungal clearance were observed in mice lacking both IL-17A and IL-17F. Clearance of C. albicans was independent of Dectin-1, Dectin-2, CARD9 (caspase-recruitment domain family, member 9), TLR2 (Toll-like receptor 2) and MyD88 in the epidermal colonization model. We found that group 3 innate lymphoid cells (ILC3s) and γδT cells were the major IL-17 producers in the epicutaneous candidiasis model. Analyses of Rag2 −/− mice and Rag2 −/− Il2rg −/− mice revealed that production of IL-17A and IL-17F by ILC3s was sufficient for C. albicans clearance. Finally, we found that depletion of neutrophils impaired C. albicans clearance in the epidermal colonization model. Taken together, these findings indicate a critical and redundant function of IL-17A and IL-17F produced by ILC3s in host defense against C. albicans in the epidermis. The results also suggest that epidermal C. albicans clearance is independent of innate immune receptors or that these receptors act redundantly in fungal recognition and clearance. [ABSTRACT FROM AUTHOR]

Intestinal microbiota dysbiosis can initiate overgrowth of commensal Candida species – a major predisposing factor for disseminated candidiasis. Commensal bacteria such as Lactobacillus rhamnosus can antagonize Candida albicans pathogenicity. Here, we investigate the interplay between C. albicans, L. rhamnosus, and intestinal epithelial cells by integrating transcriptional and metabolic profiling, and reverse genetics. Untargeted metabolomics and in silico modelling indicate that intestinal epithelial cells foster bacterial growth metabolically, leading to bacterial production of antivirulence compounds. In addition, bacterial growth modifies the metabolic environment, including removal of C. albicans' favoured nutrient sources. This is accompanied by transcriptional and metabolic changes in C. albicans, including altered expression of virulence-related genes. Our results indicate that intestinal colonization with bacteria can antagonize C. albicans by reshaping the metabolic environment, forcing metabolic adaptations that reduce fungal pathogenicity. Commensal bacteria such as Lactobacillus rhamnosus can inhibit the pathogenicity of the fungus Candida albicans. Here, Alonso-Roman et al. investigate the interplay between C. albicans, L. rhamnosus and intestinal epithelial cells, showing that changes in the metabolic environment, induced by the bacteria, trigger adaptations in C. albicans that reduce fungal pathogenicity. [ABSTRACT FROM AUTHOR]

Among the local factors for oral candidiasis, the piercing of the tongue is recognized by some authors as a risk factor for the colonization of Candida albicans. There are few case reports in which Candida spp. colonization and infection are associated with tongue piercing but only one microbiological study supports this hypothesis in general. The aim of this study was to examine this possible association between the presence of both tongue piercing and Candida spp. in healthy individuals. Positive results for tongue colonization with Candida spp. were found in four (12.9%) of the tongue-pierced subjects and in three (9.67%) subjects of the control group (p = 0.550). All samples were identified as Candida albicans. The univariate and logistic regression analyses of possible risk factors for tongue colonization revealed that gender (p = 0.024), smoking more than 10 cigarettes per day (p = 0.021), and improper hygiene (p = 0.028) were statistically significant influencing factors in the multivariate analysis. The results suggest that the piercing of the tongue is not a risk factor for colonization of Candida spp. [ABSTRACT FROM AUTHOR]

As part of the human microbiota, the fungus Candida albicans colonizes the oral cavity and other mucosal surfaces of the human body. Commensalism is tightly controlled by complex interactions of the fungus and the host to preclude fungal elimination but also fungal overgrowth and invasion, which can result in disease. As such, defects in antifungal T cell immunity render individuals susceptible to oral thrush due to interrupted immunosurveillance of the oral mucosa. The factors that promote commensalism and ensure persistence of C. albicans in a fully immunocompetent host remain less clear. Using an experimental model of C. albicans oral colonization in mice we explored fungal determinants of commensalism in the oral cavity. Transcript profiling of the oral isolate 101 in the murine tongue tissue revealed a characteristic metabolic profile tailored to the nutrient poor conditions in the stratum corneum of the epithelium where the fungus resides. Metabolic adaptation of isolate 101 was also reflected in enhanced nutrient acquisition when grown on oral mucosa substrates. Persistent colonization of the oral mucosa by C. albicans also correlated inversely with the capacity of the fungus to induce epithelial cell damage and to elicit an inflammatory response. Here we show that these immune evasive properties of isolate 101 are explained by a strong attenuation of a number of virulence genes, including those linked to filamentation. De-repression of the hyphal program by deletion or conditional repression of NRG1 abolished the commensal behaviour of isolate 101, thereby establishing a central role of this factor in the commensal lifestyle of C. albicans in the oral niche of the host. Author summary: The oral microbiota represents an important part of the human microbiota and includes several hundreds to several thousands of bacterial and fungal species. One of the most prominent fungus colonizing the oral cavity is the yeast Candida albicans. While the presence of C. albicans usually remains unnoticed, the fungus can under certain circumstances cause lesions on the lining of the mouth referred to as oral thrush or contribute to other common oral diseases such as caries. Maintaining C. albicans commensalism in the oral mucosa is therefore of utmost importance for oral health and overall wellbeing. While overt fungal growth and disease is limited by immunosurveillance mechanisms during homeostasis, C. albicans strives to survive and evades elimination from the host. Here, we show that while commensalism in the oral cavity is characterized by a restricted fungal virulence and hyphal program, enforcing filamentation in a commensal isolate is sufficient for driving pathogenicity and fungus-induced inflammation in the oral mucosa thwarting persistent colonization. Our results further support a critical role for specialized nutrient acquisition allowing the fungus to thrive in the nutrient poor environment of the squamous epithelium. Together, this work revealed key determinants of C. albicans commensalism in the oral niche. [ABSTRACT FROM AUTHOR]

Vulvovaginal candidiasis (VVC) is an infectious disease caused mainly by Candida albicans. Kangfuxin (KFX) is a traditional Chinese medicine preparation made from Periplaneta americana extracts, which promotes wound healing and enhances body immunity and also acts as an antifungal agent. Here, we evaluated the effect of KFX in the treatment of VVC in vitro and in vivo. The minimum inhibitory concentration (MIC50) of KFX against C. albicans ranged from 7·65 to 20·57%. In addition, KFX was more efficient than fluconazole (FLC) in inhibiting the drug‐resistant C. albicans, and the effect was more intense after 8 h. The KFX treatment also exhibited good activity in vivo. It restored the body weight and reduced the vulvovaginal symptoms in mice induced with VVC. It downregulated the expression of the hyphae‐related gene, HWP1, thus inhibiting the growth and development of C. albicans hyphae. It also increased the number of neutrophils and promoted the secretion of interleukin‐17A (IL‐17A); however, the levels of interleukin‐8 (IL‐8) and interleukin‐1β (IL‐1β) decreased in mice with VVC. We deduce that KFX effectively treats vaginal candidiasis in two ways: by inhibiting the growth and development of mycelia to reduce colonization of C. albicans and by promoting the secretion and release of IL‐17A and neutrophils in high numbers to fight C. albicans infection. This study provides a theoretical basis for the use of KFX for the clinical treatment of VVC. [ABSTRACT FROM AUTHOR]

Objectives: To assess the effects of benzydamine and mouthwashes (MoWs) containing benzydamine on different stages of Candida albicans biofilm: adhesion, formation, persistence, and regrowth (if perturbed). Materials and methods: C. albicans CA1398, carrying the bioluminescence ACT1p-gLUC59 fusion product, was employed. Fungal cells were exposed for 1′, 5′, or 15′ to 4 different benzydamine concentrations (0.075 to 0.6%) to 2 mouthwashes (MoWs) containing benzydamine and to a placebo MoW (without benzydamine). Treated cells were tested for adhesion (90 min) and biofilm formation (24-h assay). Next, 24- and 48-h-old biofilms were exposed to benzydamine and MoWs to assess regrowth and persistence, respectively. The effects of benzydamine, MoWs containing benzydamine, and placebo on different biofilm stages were quantified by bioluminescence assay and by the production of quorum sensing (QS) molecules. Results: Benzydamine and MoWs containing benzydamine impaired C. albicans ability to adhere and form biofilm, counteracted C. albicans persistence and regrowth, and impaired a 48-h-old biofilm. Some of these effects paralleled with alterations in QS molecule secretion. Conclusions: Our results show for the first time that benzydamine and MoWs containing benzydamine impair C. albicans capacity to form biofilm and counteract biofilm persistence and regrowth. Clinical relevance: Benzydamine and MoWs containing benzydamine capacity to affect C. albicans biofilm provides an interesting tool to prevent and treat oral candidiasis. Likely, restraining C. albicans colonization through daily oral hygiene may counteract colonization and persistence by other critical oral pathogens, such as Streptococcus mutans, whose increased virulence has been linked to the presence of C. albicans biofilm. [ABSTRACT FROM AUTHOR]

Hepatocellular carcinoma (HCC), a primary liver cancer, is closely associated with the gut microbiota. However, the role of gut fungi in the development of HCC remains unclear. The aim of this study was to explore the influence of intestinal Candida albicans on HCC. Here, We found that patients with HCC showed significantly decreased diversity of the gut mycobiome and increased abundance of C. albicans , compared to the patients with liver cirrhosis. The gavage of C. albicans in the WT models increased the tumor size and weight and influenced the plasma metabolome, which was indicated by alterations in 117 metabolites, such as L-carnitine and L-acetylcarnitine, and several KEGG enriched pathways, such as phenylalanine metabolism and citrate cycle. Moreover, the expression of nucleotide oligomerization domain-like receptor family pyrin domain containing 6 (NLRP6) in the intestinal tissues and primary intestinal epithelial cells of the WT mice interacted with C. albicans increased. Notably, the colonization of C. albicans had no effect on tumor growth in Nlrp6 –/– mice. In conclusion, the abnormal colonization of C. albicans reprogrammed HCC metabolism and contributed to the progression of HCC dependent on NLRP6, which provided new targets for the treatment of HCC. [ABSTRACT FROM AUTHOR]

Objectives: This study evaluated the incidence of Candida species, and the genetic diversity and virulence of C. albicans of the oral cavity from patients with cleft lip and palate (CLP). Materials and methods: Oral samples were investigated by microbiological and species-specific PCR methods. The genetic diversity of C. albicans was established using isoenzyme markers, Nei's statistics, and clustering analysis. Hydrolytic enzymes (SAPs and PLs) were analyzed in vitro. Results: Oral colonization by Candida species was observed in 29 patients with CLP (65.9%), and C. albicans was highly prevalent. SAP and PL activities were observed in 100% and 51.9% of isolates, respectively. High genetic diversity and patterns of monoclonal and polyclonal oral colonization by C. albicans were observed among patients with CLP. Two major polymorphic taxa (A and B) and other minor polymorphic taxa (C to J) were identified. Only one of the 16 clusters (taxon A) harbored strains from patients with and without CLP, whereas other clusters harbored strains exclusively from CLP patients. Conclusions: The anatomical conditions of the oral cavity of patients with CLP contribute to the high incidence of Candida species (C. albicans, C. krusei, C. tropicalis, and/or Candida spp.). Data suggest high genetic diversity of potentially virulent C. albicans strains in the oral cavity of CLP patients. Clinical relevance: Microbiological niches in orofacial clefts can contribute to the emergence of a relative clinical genotypic identity of C. albicans. However, orofacial rehabilitation centers can contribute to the direct and indirect sources of transmission and propagation of Candida species. [ABSTRACT FROM AUTHOR]

Candida colonisation of the oral cavity increases in immunocompromised individuals which leads to the development of oral candidiasis. In addition, host factors such as xerostomia, smoking, oral prostheses, dental caries, diabetes and cancer treatment accelerate the disease process. Candida albicans is the primary causative agent of this infection, owing to its ability to form biofilm and hyphae and to produce hydrolytic enzymes and candialysin. Although mucosal immunity is activated, from the time hyphae-associated toxin is formed by the colonising C. albicans cells, an increased number and virulence of this pathogenic organism collectively leads to infection. Prevention of the development of infection can be achieved by addressing the host physiological factors and habits. For maintenance of oral health, conventional oral hygiene products containing antimicrobial compounds, essential oils and phytochemicals can be considered, these products can maintain the low number of Candida in the oral cavity and reduce their virulence. Vulnerable patients should be educated in order to increase compliance. [ABSTRACT FROM AUTHOR]

Oral candidiasis remains a common problem in HIV-infected individuals, especially in sub-Saharan Africa. Here, we performed the first study in Chad on the prevalence of oral yeasts carriage and oral candidiasis in HIV-positive subjects from southern Chad and analyzed the influence of HAART, CD4+ T-cell numbers, and antimycotics in 589 patients. These patients were recruited from a specialized medical center for HIV patients in Sarh and from a rural medical health dispensary in the vicinity, including a total of 384 HIV-positive and 205 HIV-negative individuals. Yeasts obtained from oral specimen were identified by MALDI-TOF MS and their antifungal susceptibility profiles determined. The overall prevalence of yeast colonization and symptomatic oral candidiasis in HIV-infected patients was 25.1%. The prevalence of oral candidiasis was higher in untreated than in HAART-treated HIV-positive patients (16% vs. 2%; p < 0.01). Oral candidiasis was furthermore associated with high fungal burdens of Candida albicans and a CD4+ T-cell number <200/μl. A shift toward non -albicans Candida species was observed under nucleoside-based HAART therapy. Azole antifungal drug resistance was only observed for the intrinsically resistant species Candida krusei and Candida glabrata. Prevalence of oral candidiasis in the studied area was very low. The species distribution was similar to other countries around the world, with C. albicans being dominant. Candida dubliniensis was not isolated. Nucleoside-based HAART therapy significantly reduced oral colonization as well as occurrence of oral candidiasis caused by C. albicans and led to a species shift toward non- albicans species. Antifungal resistance was not yet a concern in Chad. [ABSTRACT FROM AUTHOR]

Background: Psoriasis patients are more frequently colonised with Candida species. The correlation between fungal colonisation and clinical severity is unclear, but may exacerbate psoriasis and the impact of antipsoriatic therapies on the prevalence of Candida is unknown. Objectives: To examine the prevalence of C species in psoriasis patients compared to an age‐ and sex‐matched control population, we investigated the influence of Candida colonisation on disease severity, immune cell activation and the interplay on psoriatic treatments. Methods: The prevalence of C species was examined in 265 psoriasis patients and 200 control subjects by swabs and stool samples for fungal cultures. Peripheral mononuclear blood cells (PBMCs) were collected from 20 fungal colonised and 24 uncolonised patients and stimulated. The expression of interferon (IFN)‐γ, IL‐17A, IL‐22 and tumour necrosis factor (TNF)‐α from stimulated PBMCs was measured by quantitative real‐time polymerase chain reaction (qPCR). Results: A significantly higher prevalence for Candida was detected in psoriatic patients (p ≤.001) compared to the control subjects; most abundant in stool samples, showing Candida albicans. Older participants (≥51 years) were more frequent colonised, and no correlation with gender, disease severity or systemic treatments like IL‐17 inhibitors was found. Conclusions: Although Candida colonisation is significantly more common in patients with psoriasis, it does not influence the psoriatic disease or cytokine response. Our study showed that Candida colonisation is particularly more frequent in patients with psoriasis ≥51 years of age. Therefore, especially this group should be screened for symptoms of candidiasis during treatment with IL‐17 inhibitors. [ABSTRACT FROM AUTHOR]

Diallyl disulfide (DADS), a garlic extract also known as allicin, has been reported to have numerous biological activities, including anticancer, antifungal, and inflammation-inhibiting activities, among others. Although many studies have assessed whether DADS can treat Candida albicans infection in vitro , its in vivo function and the underlying mechanism are still not clear. Accumulated evidence has implicated the gut microbiota as an important factor in the colonization and invasion of C. albicans. Thus, this study aimed to identify the mechanism by which DADS ameliorates dextran sulfate (DSS)-induced intestinal C. albicans infection based on the systematic analysis of the gut microbiota and metabolomics in mice. Here, we determined the body weight, survival, colon length, histological score, and inflammatory cytokine levels in the serum and intestines of experimental mice. Fecal samples were collected for gut microbiota and metabolite analysis by 16S rRNA gene sequencing and LC–MS metabolomics, respectively. DADS significantly alleviated DSS-induced intestinal C. albicans infection and altered the gut microbial community structure and metabolic profile in the mice. The abundances of some pathogenic bacteria, such as Proteobacteria , Escherichia–Shigella , and Streptococcus , were notably decreased after treatment with DADS. In contrast, SCFA-producing bacteria, namely, Ruminiclostridium , Oscillibacter , and Ruminococcaceae_UCG−013 , greatly increased in number. The perturbance of metabolites in infectious mice was improved by DADS, with increases in secondary bile acids, arachidonic acid, indoles and their derivatives, which were highly related to the multiple differentially altered metabolic pathways, namely, bile secretion, arachidonic acid metabolism, and tryptophan metabolism. This study indicated that DADS could modulate gut microbiota and metabolites and protect the gut barrier to alleviate DSS-induced intestinal C. albicans infection in mice. Moreover, this work might also provide novel insight into the treatment of C. albicans infection using DADS. [ABSTRACT FROM AUTHOR]

As a frequently occurring infectious disease mainly caused by Candida albicans, vulvovaginal candidosis (VVC) affects more than 100 million women worldwide every year. Multiple factors that influence C. albicans colonisation have been linked to the incidence of VVC, including high levels of circulating oestrogen due to pregnancy, the use of oral contraceptives, and hormone replacement therapy. This review provides an overview of the current understanding of the mechanism(s) by which oestrogen contributes to VVC, which might provide meaningful guidance to the prevention and treatment of this disease. [ABSTRACT FROM AUTHOR]

Adolescents undergoing fixed orthodontic therapy have an increased risk of oral diseases due to additional plaque accumulation sites. However, the effect of fixed orthodontics appliances (FOAs) on the colonization of Candida albicans (Ca) and Streptococcus mutans (Sm), two synergistic oral pathogens, is largely unknown and was, therefore, the primary objective of this pilot investigation. Sixteen children aged 10–15 years were enrolled, nine in the FOA and seven in the control groups. Saliva and occlusal plaque were collected, and the Ca and Sm levels were quantified with a quantitative real-time polymerase chain reaction (qPCR) assay. A trend of higher Ca levels was observed in the saliva and occlusal plaque of the FOA group, while the control group contained higher levels of Sm. Furthermore, for Sm levels, a positive correlation between saliva and occlusal plaque was shown in both the FOA and control groups; in contrast, Ca levels were negatively correlated between these samples only in the FOA group. Between Ca and Sm , a positive correlation was observed in saliva and occlusal plaque in the control group; however, this relationship was disrupted in the FOA group. Our preliminary study demonstrated that the presence of FOAs disturbs the colonization of Ca and Sm within the oral cavity. This perturbation might increase orthodontic patients' risk for Ca- and Sm -related diseases. [ABSTRACT FROM AUTHOR]

Introduction: The retentive niches of deep caries lesions have a distinct biome. Methods: We evaluated the site-specific (occlusal and proximal) Candida-biome of Severe-Early Childhood Caries (S-ECC) in 66- children (132 lesions). Asymptomatic primary molars fitting the definition of the International Caries Detection and Assessment-(ICDAS)-caries-code 5/6 were analyzed. Deep-dentinal sampling and simultaneous assessment of pH were performed. Clinical isolates were speciated using multiplex-PCR and evaluated for their acidogenic and aciduric potential.Results: Surprisingly, a high prevalence of Candida species (72.7%), either singly or in combination, was noted from both the proximal and occlusal cavities. C. tropicalis was the most prevalent species (47%; 34/72), followed by C. krusei (43.1%; 31/72) and C. albicans (40.3%; 29/72), with C. glabrata being the least (9.7%; 7/72). Over 45% low-pH niches (pH <7) of both sites yielded either dual or triple species of Candida. Genotyping revealed three distinct C. albicans genotypes (A, B, and C) with (14/29; 48.3%) of strains belonging to Genotype A. All four evaluated Candida species exhibited acidogenic and aciduric potential, C. tropicalis being the most potent.Conclusion: This, the first report of the high-density, multispecies, yeast colonization of deep-dentinal lesions in S-ECC, suggests that the Candida-biome plays a significant etiologic role in the condition, possibly due to their profound acidogenicity in milieus rich in dietary carbohydrates. [ABSTRACT FROM AUTHOR]

Denture stomatitis (DS) is one of the most common infectious diseases affecting edentulous patients, due to the colonization of candida albicans on the fitting surface dentures. Despite its multifactorial aetiology, most of the attempts at addressing this problem have been dedicated to the development of dentures or associated materials with antimicrobial activity. This review aims to provide an overview of the published literature on the development of denture base materials with antimicrobial activity and their properties. The published literature indicates that antimicrobial activity to the denture base materials was induced either by physically blending or chemically copolymerizing the antimicrobial agents into the polymeric matrix. A variety of materials such as chlorhexidine, silver and silver- based compounds, titanium dioxide nanoparticles (TiO2NP), and quaternary ammonium salts (QAS), etc., have been physically blended with the denture base materials. Antimicrobial monomers such as methacryloyloxy dodecylpyridinium bromide (MDPB), methacryloyloxy undecylpyridinium bromide (MUPB), quaternary ammonium (QA), dimethylaminododecyl methacrylate (DMADDM), 2-tert-butylaminoethyl methacrylate (TBAEMA), methacryloxylethylcetyl dimethyl ammonium chloride (DMAE-CB), acrylamide monomer (AAm), 2-methacryloxylethyl dodecyl methyl ammonium bromide (MAE-DB), 2-methacryloxylethyl hexadecyl methyl ammonium bromide (MAE-HB), 2- dimethyl-2-dodecyl-1-methacryloxyethyl ammonium iodine (DDMAI) and 2-Dimethyl-2-hexadecyl-1-methacryloxyethyl ammonium iodine (DHMAI), etc. have been copolymerized with methyl methacrylate to impart antimicrobial activity. These attempts have shown promising antimicrobial activity against C. albicans. However, significant differences in their antimicrobial activity as well as in their properties were noted. Incorporation of antimicrobial monomers to PMMA denture base resin decreased the biofilm formation with a consequent reduction in the acid production and metabolic activity of microbes. Such modifications showed promise as possible alternatives against Candida associated denture stomatitis. [ABSTRACT FROM AUTHOR]

The commensal and opportunistic pathogen Candida albicans is an important cause of fungal diseases in humans, with the gastrointestinal tract being an important reservoir for its infections. The study of the mechanisms promoting the C. albicans commensal state has attracted considerable attention over the last few years, and several studies have focused on the identification of the intestinal human mycobiota and the characterization of Candida genes involved in its establishment as a commensal. In this work, we have barcoded 114 clinical C. albicans isolates to identify strains with an enhanced fitness in a murine gastrointestinal commensalism model. The 114 barcoded clinical isolates were pooled in four groups of 28 to 30 strains that were inoculated by gavage in mice previously treated with antibacterial therapy. Eight strains that either exhibited higher colonization load and/or remained in the gut after antibiotic removal were selected. The phenotypic analysis of these strains compared to an RFP-tagged SC5314 wild type strain did not reveal any specific trait associated with its increased colonization; all strains were able to filament and six of the eight strains displayed invasive growth on Spider medium. Analysis of one of these strains, CaORAL3, revealed that although mice required previous bacterial microbiota reduction with antibiotics to be able to be colonized, removal of this procedure could take place the same day (or even before) Candida inoculation. This strain was able to colonize the intestine of mice already colonized with Candida without antibiotic treatment in co-housing experiments. CaORAL3 was also able to be established as a commensal in mice previously colonized by another (CaHG43) or the same (CaORAL3) C. albicans strain. Therefore, we have identified C. albicans isolates that display higher colonization load than the standard strain SC5314 which will surely facilitate the analysis of the factors that regulate fungal colonization. [ABSTRACT FROM AUTHOR]

Masking the immunogenic cell wall epitope ß(1,3)-glucan under an outer layer of mannosylated glycoproteins is an important virulence factor deployed by Candida albicans during infection. Consequently, increased ß(1,3)-glucan exposure (unmasking) reveals C. albicans to the host's immune system and attenuates its virulence. We have previously shown that activation of the Cek1 MAPK pathway via expression of a hyperactive allele of an upstream kinase (STE11ΔN467) induces unmasking. It also increased survival of mice in a murine disseminated candidiasis model and attenuated kidney fungal burden by ≥33 fold. In this communication, we utilized cyclophosphamide-induced immunosuppression to test if the clearance of the unmasked STE11ΔN467 mutant was dependent on the host immune system. Suppression of the immune response by cyclophosphamide reduced the attenuation in fungal burden caused by the STE11ΔN467 allele. Moreover, specific depletion of neutrophils via 1A8 antibody treatment also reduced STE11ΔN467-dependent fungal burden attenuation, but to a lesser extent than cyclophosphamide, demonstrating an important role for neutrophils in mediating fungal clearance of unmasked STE11ΔN467 cells. In an effort to understand the mechanism by which Ste11ΔN467 causes unmasking, transcriptomics were used to reveal that several components in the Cek1 MAPK pathway were upregulated, including the transcription factor CPH1 and the cell wall sensor DFI1. In this report we show that a cph1ΔΔ mutation restored ß(1,3)-glucan exposure to wild-type levels in the STE11ΔN467 strain, confirming that Cph1 is the transcription factor mediating Ste11ΔN467-induced unmasking. Furthermore, Cph1 is shown to induce a positive feedback loop that increases Cek1 activation. In addition, full unmasking by STE11ΔN467 is dependent on the upstream cell wall sensor DFI1. However, while deletion of DFI1 significantly reduced Ste11ΔN467-induced unmasking, it did not impact activation of the downstream kinase Cek1. Thus, it appears that once stimulated by Ste11ΔN467, Dfi1 activates a parallel signaling pathway that is involved in Ste11ΔN467-induced unmasking. Author summary: Candida albicans is a significant cause of fungal bloodstream infections. Yet, in order for it to effectively induce disease, host immune evasion must be achieved. C. albicans often accomplishes this by masking structures within its cell wall that are recognized by the host immune system, such as ß(1,3)-glucan. Thus, inappropriately exposing (unmasking) this epitope may be a way to increase immune system recognition of invading fungal cells to enhance host clearance. We have previously shown that we can induce inappropriate unmasking in C. albicans by regulated expression of a hyperactive mutant of the MAP3K STE11 of the Cek1 MAPK pathway, and that this reduces fungal colonization during systemic infection in mice. We hypothesized that the observed virulence attenuation was a consequence of enhanced host immune system recognition caused by unmasking induced by the canonical Cek1 MAPK pathway. In this report, we found that Ste11ΔN467-induced unmasking was indeed mediated by one of its known downstream transcription factors, Cph1, and that its virulence attenuation in vivo was largely dependent on a functional immune response. Thus, leveraging the Cek1 pathway may serve as a model to study how unmasking occurs in C. albicans, and how the host responds to this phenotype in vivo. [ABSTRACT FROM AUTHOR]

Candida albicans is the main fungal species associated with the development of oral candidiasis. Currently, therapeutic options for these infections are limited by the adverse effects of antifungal drugs and by the emergence of drug resistant strains. Thus, the development of new antifungal agents is needed for the prevention and treatment of oral Candida infections. Caffeic acid phenethyl ester (CAPE) is a natural compound from propolis polyphenolic groups that exhibits many pharmacological properties. In this study, we investigated whether CAPE can have antifungal and immunomodulatory effects on oral candidiasis. Preliminary tests to assess the antifungal activity of CAPE were performed using the Minimum Inhibitory Concentration (MIC) assay that demonstrated inhibition in a range from 16 to 32 μg/mL, confirming its antifungal activity on several C. albicans strains isolated from the oral cavity. Subsequently, we analyzed Candida spp biofilms formed in vitro , in which CAPE treatment at 5 x MIC caused a reduction of 68.5% in the total biomass and ~2.60 Log in the viable cell count (CFU/mL) in relation to the untreated biofilm (p <0.0001). Next, RNA was extracted from untreated and CAPE-treated biofilms and analyzed by real-time qPCR. A series of genes analyzed (ALS1, ECE1, EPA1, HWP1 , YWP1, BCR1, BGR1, CPH1, EFG1 , NDT80, ROB1, TEC1 , UME6 , SAP2 , SAP5 , PBL2 , and LIP9) were downregulated by CAPE compared to the untreated control group (p <0.0001). In in vivo studies using Galleria mellonella , the treatment with CAPE prolonged survival of larvae infected by C. albicans by 44.5% (p < 0.05) and accompanied by a 2.07-fold increase in the number of hemocytes. Flow cytometry revealed the most prominent increases were in types P2 and P3 hemocytes, granular cells, which phagocytize pathogens. In addition, CAPE treatment decreased the fungal load in the hemolymph and stimulated the expression of antifungal peptide genes such as galiomicin and gallerimycin. The antifungal and immunomodulatory activities observed in G. mellonella were extended to a murine model of oral candidiasis, in which CAPE decreased the levels of C. albicans colonization (~2 log CFU/mL) in relation to the untreated control group. In addition, CAPE treatment significantly reduced pseudomembranous lesions, invasion of hyphae on epithelium surfaces, tissue damage and inflammatory infiltrate (p < 0.05). CAPE was also able to increase the expression of β-defensin 3 compared to the infected and untreated group by 3.91-fold (p < 0.0001). Taken together, these results show that CAPE has both antifungal and immunomodulatory effects, making it a promising natural antifungal agent for the treatment and prevention of candidiasis and shows impact to oral candidiasis. [ABSTRACT FROM AUTHOR]

I pylori i may induce a stress response that activate the formation of volutin granules in the vacuoles of I C i . I pylori i were abundant in certain human niches, such as the root canal necrotic pulp, stomach, duodenum, and vagina [[6]], suggesting that I C i . I pylori i in different environmental conditions to promote its pathogenicity and transmission (Fig 1), since I C i . I pylori i to promote the growth, spread, and infection of I H i . [Extracted from the article]

Candida albicans is a major fungal pathogen of humans. It exists as a commensal in the oral cavity, gut or genital tract of most individuals, constrained by the local microbiota, epithelial barriers and immune defences. Their perturbation can lead to fungal outgrowth and the development of mucosal infections such as oropharyngeal or vulvovaginal candidiasis, and patients with compromised immunity are susceptible to life-threatening systemic infections. The importance of the interplay between fungus, host and microbiota in driving the transition from C. albicans commensalism to pathogenicity is widely appreciated. However, the complexity of these interactions, and the significant impact of fungal, host and microbiota variability upon disease severity and outcome, are less well understood. Therefore, we summarise the features of the fungus that promote infection, and how genetic variation between clinical isolates influences pathogenicity. We discuss antifungal immunity, how this differs between mucosae, and how individual variation influences a person's susceptibility to infection. Also, we describe factors that influence the composition of gut, oral and vaginal microbiotas, and how these affect fungal colonisation and antifungal immunity. We argue that a detailed understanding of these variables, which underlie fungal-host-microbiota interactions, will present opportunities for directed antifungal therapies that benefit vulnerable patients. [ABSTRACT FROM AUTHOR]