Search

This research endeavors to investigate the potential preventive and protective effects of chlorogenic acid (CGA), a bioactive component found in various foods, in the context of dextran sodium sulfate (DSS)-induced colitis in mice. The study reveals that CGA administration, at dosages of 150 and 300 mg/kg, significantly retards the progression of colitis. This is substantiated by observable enhancements in colon length, reduction in the disease activity index, and mitigation of colon tissue damage. Meanwhile, CGA acts as an antioxidant by reducing the oxidative stress associated with colitis inflammation and increasing the activity of antioxidant enzymes. Furthermore, CGA demonstrates anti-inflammatory properties by inhibiting the inflammatory response associated with colitis and regulating the excessive expression of cytokines. Notably, CGA contributes to the restoration of intestinal barrier function by augmenting the levels of claudin-1 and ZO-1. Moreover, the investigation uncovers CGA's capacity to modulate the gut microbiota composition in colitic mice, fostering the proliferation of beneficial bacteria, notably Lactobacillus , while concurrently impeding the growth of detrimental bacteria like Bacteroides , Enterobacteriaceae, and Escherichia_Shigella. To conclude, these findings substantiate the viability of CGA for diverse applications in the realms of food and medicine, thereby bolstering its potential as a therapeutic strategy within dietary interventions. [ABSTRACT FROM AUTHOR]

Allergic asthma accounts for more than 50 percent of adult asthma in life. Glucocorticoids and leukotriene receptor antagonists are commonly used to treat asthma, but these drugs not only have high side effects but also cannot cure the disease. In contrast, natural active ingredients are relatively safe to the organism and show great potential for improving the organism. Polysaccharides, as the main active ingredient in aqueous extract, may be equally beneficial for biological activity. The aim of this study is to investigate the alleviating effect and mechanism of action of Ficus pumila fruit polysaccharide (FPP) and aqueous extract of Ficus pumila fruit (FPW) on mice with allergic asthma. The results showed that FPP and FPW could regulate the secretion of the cytokines IL-4, IL-5, IL-13, and IFN-γ. FPP and FPW also reduced the inflammation, mucus secretion, and collagen deposition in mouse lung tissue, and down-regulated the expression of matrix metallopeptidase-9 (MMP-9), tissue inhibitor of metalloproteinases-1 (TIMP-1), and α-smooth muscle actin (α-SMA) proteins. In addition, FPP and FPW modulated the intestinal microbiota by augmenting the alpha diversity and adjusting the taxonomic composition at the phylum and family levels, thereby ensured the sustenance of regular physiological processes in the body. This study demonstrated that FPP and FPW may attenuate asthma by inducing beneficial microbiota in the gut-lung axis and provide an effective basis for the future clinical treatment of allergic asthma with Ficus pumila and the development and utilization of new anti-asthma drugs. [Display omitted] • Ficus pumila fruit could effectively alleviate the symptoms of allergic asthma mice. • Ficus pumila fruit also reduced the inflammation, mucus secretion, and collagen deposition in mouse lung tissue. • Ficus pumila fruit polysaccharide maintained the balance of gut flora and promoted the production of short-chain fatty acids. • Ficus pumila fruit polysaccharide could upregulate the diversity of gut microbial. [ABSTRACT FROM AUTHOR]

Western honey bee (Apis mellifera) is widely used in investigations involved in gut flora, and the gut flora of their workers have been demonstrated to be completely colonized within 7 days of emergence. However, colonization rules of the gut flora remain largely unknown. Here, metagenomic 16S rRNA gene data were generated to study colonization rules of the gut flora in workers by detecting dynamics in diversity and the relative abundance of gut bacteria across 14 time points post-emergence from pupal case, including 0 pupation-hours/control, 12, 24, 36, 48, 60, 72, 84, 96, 108, 120, 132, 144, and 156 post-emergence-hours (peh). Via comparison analysis of bacterial operational taxonomic units across these time points, diversity values of the gut flora presented the maximum at 0 peh. Among these points, 0–24 peh maintained the relatively higher diversity than the other time points. Furthermore, dynamic changes in several core gut bacteria (e.g., Lactobacillus, Bifidobacterium, Frischella, Snodgrassella, and Gilliamella) were analyzed in detail, and their biological function was linked to several host biological characteristics such as ecological adaptation, aging, gut health, dietary alterations and diversity, digestion and absorption, and metabolisms during colonization. This study is valuable for the understanding of colonization rules and the contribution of the gut flora to workers. [ABSTRACT FROM AUTHOR]

Fusobacterium nucleatum , which is involved in the development of periodontal disease and apical lesions, can be transmitted to the colon and metastasize to colorectal cancer, suggesting a link between oral and systemic diseases. We analyzed the effects of F. nucleatum on bacterial flora in the gut and surrounding organs in a rat model of apical periodontitis and analyzed the infection route to the gut and distant organs. We induced apical periodontitis in rat molars by infecting the dental pulp with F. nucleatum and then took X-ray images and performed histopathologic analyses. Next, we removed the maxilla, gut, heart, liver, and kidney from the rats at 0, 2, 4, and 8 weeks postsurgery and then extracted DNA samples and performed polymerase chain reaction and microbiome analyses using the Illumina MiSeq (Illumina Co, Tokyo, Japan). The presence of inflammatory cell infiltration confirmed apical periodontitis from 2–8 weeks. Polymerase chain reaction and microbiome analyses revealed F. nucleatum in the rat gut from 2 weeks and in the kidney from 8 weeks. The rat gut, heart, liver, and kidney exhibited altered bacterial flora, including a marked decrease in Verrucomicrobia and an increase in Proteobacteria after 2 weeks and increases in Bacteroidetes and Firmicutes after 4 weeks. The onset of F. nucleatum –induced apical periodontitis changed the bacterial flora in the rat gut, heart, liver, and kidney, with a confirmed progressing infection in the large intestines. [ABSTRACT FROM AUTHOR]

Intestinal barrier dysfunction is a significant contributor to the recurrence and refractory of ulcerative colitis (UC). Promoting the interaction between group 3 innate lymphoid cells (ILC3s) and gut flora is a valuable strategy for mucosal repair. Paeoniae decoction (PD) is a compound commonly used in clinical treatment of UC, but its exact mechanism remains unclear. We aimed to investigate the protective effect of PD on intestinal mucosal injury induced by dextran sulfate sodium (DSS) in chronic colitis, as well as to elucidate its potential mechanism. C57BL/6 mice were induced with chronic colitis by 2 % DSS and divided into four groups: control group, model group, PD low dose (4 g/kg), and high dose (8 g/kg) group. The effectiveness of PD in treating chronic colitis mice was evaluated based on changes in body weight, colon length, colon pathological tissue scores, and the mRNA levels of inflammatory factors IL-6 and IL-1β. The expressions of intestinal epithelial tight junction proteins (ZO-1 and Occludin), IL-22, and MUC2 were observed using immunofluorescence and RT-PCR. Additionally, the proportion of ILC3 and natural cytotoxicity receptor (NCR)+ ILC3 in the colon were detected using flow cytometry. Furthermore, UHPLC-QE-MS was utilized to identify chemical components of PD and network pharmacology was employed to predict potential pathways for PD intervention in UC. Subsequently, MNK-3 cells (ILC3 in vitro cell line) and NCM460 cells were used to verify the network pharmacology results. Finally, the effects of PD on UC gut flora have been explored using in vitro fermentation and 16S rDNA techniques. The results showed that PD significantly restored body weight and colon length in mice with chronic colitis, while also reducing colon inflammatory cell infiltration and the expression of IL-6 and IL-1β. Additionally, PD notably promoted the expression of MUC2, ZO-1, Occludin, and IL-22, as well as increasing the ratio of ILC3 and NCR+ILC3. UHPLC-QE-MS analysis identified 443 components of PD, and network pharmacology suggested that PD could target the aryl hydrocarbon receptor (AHR) signaling pathway, which was confirmed by MNK-3 cells and in vitro fermentation experiments. Furthermore, MNK-3-conditioned medium (CM) increased the expression of ZO-1 and Occludin in NCM460 cells. In addition, 16S rDNA results indicated that PD promoted the abundance of Lactobacillales , thus contributing to mucosal damage repair by activating the AHR signal in ILC3s. In summary, our study demonstrates that PD repairs intestinal mucosal damage in chronic colitis by regulating the interaction of gut flora with ILC3, and the specific mechanism is related to the activation of AHR signaling pathway. [Display omitted] [ABSTRACT FROM AUTHOR]

• Flavonoids of C. Nudiflora is the potential drugs for the treatment of colitis. • Flavonoids of C. Nudiflora recoveres intestinal damage in mice. • Flavonoids of C. Nudiflora regulates the structure of intestinal flora. • Flavonoids of C. Nudiflora regulates NF-κB and MAPK pathways. Callicarpa nudiflora Hook (C. nudiflora) is an anti-inflammatory, antimicrobial, antioxidant, and hemostatic ethnomedicine. To date, little has been reported regarding the activity of C. nudiflora against ulcerative colitis (UC). In this study, we investigated the effect of a flavonoid extract of C. nudiflora on Dextran Sulfate Sodium (DSS)-induced ulcerative colitis in mice. Mice in the treatment group (CNLF+DSS group) and drug-only (CNLF group) groups were administered 400 mg/kg of flavonoid extract of C. nudiflora leaf (CNLF), and drinking water containing 2.5 % DSS was given to the model and treatment groups. The symptoms of colitis were detected, relevant indicators were verified, intestinal barrier function was assessed, and the contents of the cecum were analyzed for intestinal microorganisms. The results showed that CNLF significantly alleviated the clinical symptoms and histological morphology of colitis in mice, inhibited the increase in pro-inflammatory factors (TNF-α, IL-6, IL-1β, and IFN-γ), and increased the level of IL-10. The expression of NF-κB and MAPK inflammatory signal pathway-related proteins (p-p65, p-p38, p-ERK, p-JNK) was regulated. The expression of tight junction proteins (ZO-1, OCLDN, and CLDN1) was increased, while the content of D-LA, DAO, and LPS was decreased. In addition, 16S rRNA sequencing showed that CNLF restored the gut microbial composition, and increased the relative abundance of Prevotellaceae, Intestinimonas butyriciproducens , and Barnesiella_intestinihominis. In conclusion, CNLF alleviated colitis by suppressing inflammation levels, improving intestinal barrier integrity, and modulating the intestinal microbiota, and therefore has promising future applications in the treatment of UC. [ABSTRACT FROM AUTHOR]

Microplastics (MPs), which are prevalent and increasingly accumulating in aquatic environments. Other pollutants coexist with MPs in the water, such as pesticides, and may be carried or transferred to aquatic organisms, posing unpredictable ecological risks. This study sought to assess the adsorption of lambda-cyhalothrin (LCT) by virgin and aged polyethylene MPs (VPE and APE, respectively), and to examine their influence on LCT's toxicity in zebrafish, specifically regarding acute toxicity, oxidative stress, gut microbiota and immunity. The adsorption results showed that VPE and APE could adsorb LCT, with adsorption capacities of 34.4 mg∙g−1 and 39.0 mg∙g−1, respectively. Compared with LCT exposure alone, VPE and APE increased the acute toxicity of LCT to zebrafish. Additionally, exposure to LCT and PE-MPs alone can induce oxidative stress in the zebrafish gut, while combined exposure can exacerbate the oxidative stress response and intensify intestinal lipid peroxidation. Moreover, exposure to LCT or PE-MPs alone promotes inflammation, and combined exposure leads to downregulation of the myd88-nf-κb related gene expression, thus impacting intestinal immunity. Furthermore, exposure to APE increased LCT toxicity to zebrafish more than VPE. Meanwhile, exposure to PE-MPs and LCT alone or in combination has the potential to affect gut microbiota function and alter the abundance and diversity of the zebrafish gut flora. Collectively, the presence of PE-MPs may affect the toxicity of pesticides in zebrafish. The findings emphasize the importance of studying the interaction between MPs and pesticides in the aquatic environment. • Microplastics adsorb Lambda-cyhalothrin and become the carrier of Lambda-cyhalothrin. • Microplastics enhanced the acute toxicity of Lambda-cyhalothrin to zebrafish. • Combined exposure inhibited oxidative stress and exacerbates lipid peroxidation. • Single and combined exposures led to changes in intestinal flora richness as well as diversity. • Combined exposure produced immunotoxicity. [ABSTRACT FROM AUTHOR]

Parkinson's disease (PD) is a neurodegenerative condition characterized by the progressive loss of dopaminergic neurons within the substantia nigra. Neuroinflammation plays a pivotal role in the pathogenesis of PD, involving the activation of microglia cells, heightened production of proinflammatory cytokines, and perturbations in the composition of the gut microbiota. Rubusoside (Ru), the principal steviol bisglucoside present in Rubus chingii var. suavissimus (S.K.Lee) L.T.Lu (Rosaceae), has been documented for its anti-inflammatory properties in diverse disease models. Nonetheless, there is an imperative need to comprehensively assess and elucidate the protective and anti-inflammatory attributes of Ru concerning PD, as well as to uncover the underlying mechanism involved. The aim of this study is to evaluate the neuroprotective and anti-inflammatory effects of Ru on PD and investigate its potential mechanisms associated with microbes. We pre-treated mice and cell lines with Ru in order to simulate the progression of PD and the neuroinflammatory state. The mouse model was induced by 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP), SN4741 cells were induced by 1-methyl-4-phenylpyridine (mpp+), and BV-2 cells were induced by lipopolysaccharide (LPS). We assessed the impact of Ru on motor function, neuroinflammation, neuron apoptosis, the composition of gut microbes, and their metabolites. Ru treatment reduces the release of pro-inflammatory mediators by inhibiting microglia activation. It also prevents neuronal apoptosis, thereby safeguarding dopaminergic neurons and ameliorating motor dysfunction. Furthermore, it induces alterations in the fecal microbiota composition and metabolites profile in PD mice. In vitro experiments have demonstrated that Ru inhibits neuronal apoptosis in SN4741 cells induced by mpp+, suppresses the production of pro-inflammatory mediators, and activates the c-Jun N-terminal kinase (JNK), mitogen-activated protein kinase (p38 MAPK), and nuclear factor kappa-B (NF-κB) signaling pathways. Ru exhibits inhibitory effects on the MPTP-induced PD model by mitigating neuroinflammation and neuronal apoptosis while also inducing changes in the gut microbiota and metabolite composition. [Display omitted] [ABSTRACT FROM AUTHOR]

[Display omitted] • SK hydrogel as vehicle for Cur delivery to colon exerts potential therapeutic effect. • SK-Cur relieves clinical symptoms in DSS-induced UC mice more effectively than Cur. • SK-Cur ameliorates colitis by regulating oxidative stress and inflammatory responses. • SK-Cur modulates the gut flora community of mice being similar to normal state. Scallop (Patinopecten yessoensis) male gonad hydrolysates/ κ -carrageenan (SK) double cross-linking network hydrogels were constructed as curcumin (Cur) delivery vehicles with good gel mechanical property and homogeneous honeycomb microstructures. Compared with Cur + DSS group, weight loss and colon length in SK-Cur + DSS group increased about 1.04 and 1.06 folds, while the disease active index (DAI) scores decreased about 13 %. Moreover, SK-Cur showed superior effect on intestinal barrier improvement, oxidative stress modulation, and inflammatory expression regulation, reflected by 1.1 folds increment of epithelial tight junction proteins, 16 % and 27 % decline in MPO and iNOS levels, 20 % decline in NF-κB expression, 4 %, 7 %, 6 % decline in TNF-α, IL-1β, IL-6 expression in serum, and 9 %, 20 %, 7 % decline in TNF-α, IL-1β, IL-6 expression in colon tissue. Furthermore, SK-Cur enriched alpha diversity and restored taxonomic composition with increasing Bacteroides and Verrucomicrobia abundance accompanied by decreasing Firmicutes in DSS-induced UC mice, roughly to a normal gut flora state. [ABSTRACT FROM AUTHOR]

Background: Hypericum attenuatum Choisy, a traditional Chinese herb, has been shown to be effective in the treatment of diseases associated with inflammation and has been used to treat rheumatic arthritis in China for centuries. However, the underlying mechanism of its anti-inflammatory effect is poorly understood.Hypothesis/purpose: In this study, we aimed to investigate the anti-inflammatory mechanisms of EtOAc fractions of H. attenuatum Choisy (Ha-EtOAc) on lipopolysaccharide (LPS)-induced RAW264.7 macrophage inflammation and hypothesized that Ha-EtOAc could attenuate inflammation in the colon.Study Design: LPS was utilized to induce RAW264.7 cells inflammation. The anti-inflammatory effect of Ha-EtOAc in RAW264.7 cells was evaluated by measuring the inhibition ratio of nitric oxide (NO) production. Murine ulcerative colitis (UC) was induced by treatment with 2.5% dextran sulfate sodium (DSS). The basic indexes of the mice, including body weight, food intake and hematochezia, were recorded during mice experiments.Methods: The expression levels of pro-inflammatory cytokines, including TNF-α, IL-6 and IL-1β, were measured by quantitative real-time PCR and western blot. Additionally, the influences of Ha-EtOAc on the NF-κB and MAPK signaling pathways were determined by western blot and immunofluorescence assays. In addition, the impact of Ha-EtOAc on gut microbiota of mice with UC was detected by 16S rDNA sequencing.Results: Ha-EtOAc inhibited the LPS-induced production of NO and decreased the release of TNF-α, IL-6 and IL-1β in RAW264.7 cells in a dose-dependent manner. In addition, pretreatment with Ha-EtOAc could suppress the nuclear translocation of p65 and the phosphorylation of Erk1/2, p38 and JNK. Ha-EtOAc treatment ameliorated murine UC, as reflected by a reduced body weight loss, improved colon shortening, alleviated mucosal damage and decreased releases of pro-inflammatory cytokines. Furthermore, Ha-EtOAc could modulate the composition of microbial communities.Conclusion: Our results demonstrated that Ha-EtOAc exhibited anti-inflammatory effects mainly by suppressing the NF-κB and MAPK pathways, and Ha-EtOAc treatment may be a potent therapy for the treatment of ulcerative colitis. [ABSTRACT FROM AUTHOR]

[Display omitted] • We analyzed the effect of W. coagulans SANK70258 +/− GOS on skin and bowel condition. • Skin roughness and scaliness were significantly improved by the symbiotic treatment. • Symbiotic treatment reduced p-cresol production in feces. • Symbiotic treatment reduced the amount of genera correlated with p-cresol content. • Improving the intestinal environment may partly improve skin condition. In this study, we evaluate the effects of Weizmannia coagulans SANK70258 intake on skin condition and defecation, both alone and in combination with galacto-oligosaccharides, by conducting a randomized, double-blind, parallel-group, placebo-controlled, eight-week study of 45 healthy individuals. The primary endpoints were measurement of the stratum corneum moisture content, transepidermal water loss, and skin texture; the secondary endpoints were skin assessment, a defecation survey, and measurement of fecal organic acid and p-cresol contents. The participants were divided into a W. coagulans SANK70258 alone (lac + dex) group, a W. coagulans SANK70258 plus galacto-oligosaccharides (lac + gal) group, and a placebo (dex) group. The lac + gal group showed a decrease in skin roughness and fecal p-cresol content. Scaliness was improved in lac + dex and lac + gal groups. Thus, synbiotics combining W. coagulans SANK70258 and galacto-oligosaccharides can improve scaliness and skin roughness and reduce fecal p-cresol content. [ABSTRACT FROM AUTHOR]

The larvae of the black soldier fly, Hermetia illucens , are now attracting attention and becoming promising sources for aquafeed ingredient due to the nutritious substance. However, the introduction of a novel ingredient into the recipe may have unpredictable effects on the innate immune function and gut bacteria composition of crustaceans. Therefore, the present study aimed to evaluate how dietary black soldier fly larvae meal (BSFLM) affected the antioxidant ability, innate immunity and gut microbiome of shrimp (Litopenaeus vannamei) fed with a practical diet, including the gene expression of Toll and immunodeficiency (IMD) pathways. Six experimental diets were formulated by replacing gradient levels of fish meal (0 %, 10 %, 20 %, 30 %, 40 % and 50 %) based on a commercial shrimp diet. Four replicates of shrimp were fed different diets three times daily for 60 days. Growth performance linearly decreased with increasing BSFLM inclusion. Results of antioxidative enzyme activities and gene expression suggested that low dietary BSFLM levels activated the antioxidant capacity of shrimp, while dietary BSFLM levels up to 100 g/kg may induce oxidative stress and inhibit glutathione peroxidase activity. Although traf6 , toll1 , dorsal and relish were significantly upregulated in different BSFLM groups, the expression of tak1 was significantly downregulated in groups containing BSFLM, implying the immune susceptibility may be weakened. Gut flora analysis indicated dietary BSFLM altered both beneficial and opportunistic pathogenic bacterial abundance, with low levels of dietary BSFLM increased the abundance of bacteria that may contribute to carbohydrate utilization, while high levels of dietary BSFLM may cause intestinal disease and low intestinal immune response. To conclude, 60–80 g/kg of dietary BSFLM showed no adverse effects on the growth, antioxidant capacity and gut flora of shrimp, which was the adequate level in shrimp diet. While 100 g/kg dietary BSFLM may induce oxidative stress and potentially weaken the innate immunity of shrimp. [Display omitted] • 60-80 g/kg of dietary BSFLM was an adequate level in shrimp diet. • 100 g/kg of dietary BSFLM may induce some pathogenic gut bacteria and weaken the innate immunity of shrimp. • The addition of BSFLM in commercial shrimp diets should be careful. [ABSTRACT FROM AUTHOR]

[Display omitted] • Four carbon sources derived from Pyrus bretschneideri Rehd. affect the growth of microorganisms associated with obesity. • Different gut microorganisms are correlated with short-chain fatty acids. • Anaerostipes used lactic acid and acetic acid as substrates to produce butyric acid. Nutrients such as dietary fiber in Pyrus bretschneideri Rehd. (PBR), which is mainly produced on the Tibetan Plateau, can be used as a fermentable carbon source for microorganisms. However, the mechanisms by which different carbon sources interact with microorganisms and their fermentation metabolites are not clear. In this study, four different carbon sources extracted from PBR were used to explore the effect of carbon source type on gut flora (GF) and the metabolites thereof through an in vitro simulated colonic fermentation model. The results showed a differentiation of the type of carbon source on the species composition and structure of GF, as well as on the production of metabolites during in vitro fermentation. Correlations between some microbial taxa and their metabolites were also revealed, such as Subdoligranulum and acetic acid, Collinsella and propionic acid, and Fusicatenibacter and butyric acid showing significant positive correlations. Notably, a cross-feeding pathway was clarified: Anaerostipes uses lactic acid and acetic acid as substrates to produce butyric acid. Overall, this study provided insight into the effects of different carbon sources from PBR as fermentation substrates on GF growth and metabolism, which could provide a basis for exploring the relationship between carbon source types, GF and their metabolites, and promote the integrated development of PBR resources in Qinghai Province. [ABSTRACT FROM AUTHOR]

This systematic review of animal studies aimed to identify anti-obesity medicinal herbs with prebiotic properties, and investigate their effects on gut microbiota and metabolic disorders. To obtain the relevant publications, four electronic databases were systematically searched up to June 2019. Out of 1949 publications, 20 articles met the inclusion criteria in this study. Apart from body weight, some cases (n = 11) had reported the effects of medicinal herbs on metabolic parameters, including lipid profile (n = 7) and glycemic status (n = 4). Although some medicinal herbs could be effective in modulating metabolic status and body weight, through making changes in the gut flora, further studies are needed to confirm the efficacy of such herbs in clinical trials. • Garcinia brasiliensis , Grifolafrondosa , Ganodermalucidum , Eugenia Jambolana Lam., can increase the production of short chain fatty acids. • Green coffee, Pu-erh tea, Ganodermalucidum, Chlorella pyrenoidosa, and Polygala tenuifolia can affect obesity. • Some herbs can reduce glucose level through changes in microbiota composition. [ABSTRACT FROM AUTHOR]

Abstract: At the “5th International Meeting on Inflammatory Bowel Diseases selected topics of inflammatory bowel disease (IBD), including the environment, genetics, the gut flora, the cell response and immunomodulation were discussed in order to better understand specific clinical and therapeutic aspects. The incidence of IBD continues to rise, both in low and in high-incidence areas. It is believed that factors associated with ‘Westernization’ may be conditioning the expression of these disorders. The increased incidence of IBD among migrants from low-incidence to high-incidence areas within the same generation suggests a strong environmental influence. The development of genome-wide association scanning (GWAS) technologies has lead to the discovery of more than 100 IBD loci. Some, as the Th 17 pathway genes, are shared between Crohn''s disease (CD) and ulcerative colitis (UC), while other are IBD subtype-specific (autophagy genes, epithelial barrier genes). Disease-specific therapies targeting these pathways should be developed. Epigenetic regulation of the inflammatory response also appears to play an important role in the pathogenesis of IBD. The importance of gut flora in intestinal homeostasis and inflammation was reinforced, the concepts of eubiosis and dysbiosis were introduced, and some strategies for reverting dysbiosis to a homeostatic state of eubiosis were proposed. The current status of studies on the human gut microbiota metagenome, metaprotome, and metabolome was also presented. The cell response in inflammation, including endoplasmic reticulum (ER) stress responses, autophagy and inflammasome-dependent events were related to IBD pathogenesis. It was suggested that inflammation-associated ER stress responses may be a common trait in the pathogenesis of various chronic immune and metabolic diseases. How innate and adaptive immunity signaling events can perpetuate chronic inflammation was discussed extensively. Signal transduction pathways provide intracellular mechanisms by which cells respond and adapt to multiple environmental stresses. The identification of these signals has led to a greater mechanistic understanding of IBD pathogenesis and pointed to potentially new therapeutic targets. A critical analysis of clinical trials and of risk-benefit of biological therapy was presented. The problem of Epstein–Barr virus (EBV) and lymphoma in IBD was extensively discussed. Lymphomas can develop in intestinal segments affected by IBD and are in most cases associated with EBV. The reasons of treatment failure were also analyzed both from basic and clinical points of view. Two very interesting presentations on the integration of research and clinical care in the near future closed the meeting. These presentations were focused on macrotrends affecting healthcare delivery and research, and the need to innovate traditional infrastructures to deal with these changing trends as well as new opportunities to accelerate scientific knowledge. [Copyright &y& Elsevier]

A fragrant, spherical, osmotrophic eukaryote was isolated 27 times from the digestive tracts of marine invertebrates collected from the Northeast Pacific. The isolates were cultured from 7 animal collections over a 2-year period, most from the peanut worm, Phascolosoma agassizii. A small subunit ribosomal DNA phylogeny placed the spherical organism within the ichthyosporea, closest to Sphaeroforma arctica and Pseudoperkinsus tapetis. Supporting the close relationship of isolates, the sequences of ribosomal gene internal transcribed spacers determined for 26 isolates were identical, as were the elongation factor 1-alpha-like gene fragments from 7 isolates. Dispersal via amoeboid cells distinguished this species from its closest relatives and led to the erection of a new genus and species, “Creolimax fragrantissima.” Vegetative cells reproduced asexually in vitro after they reached 30–60μm in diameter by producing amoebae or endospores, which escaped through openings in the parent cell wall. Ultrathin sections of vegetative cells prepared by high-pressure-freeze substitution provided some of the first images of ichthyosporean spindle pole bodies and document, for the first time, tubular extensions of the plasma membrane into an electron-translucent inner layer of the cell wall. Ichthyosporeans are parasites and commensals of animals and culturable species are few. Because “C. fragrantissima” can be isolated regularly and repeatedly from nature and then grown easily through cycles of asexual reproduction, it has the potential to serve as a model organism for further research into marine ichthyosporeans. [Copyright &y& Elsevier]

Copyright of Komplementaere und Integrative Medizin is the property of Elsevier B.V. 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.)

A modern approach to inflammatory bowel disease (IBD) research has been under way for little over one-half century, but only during the last two decades has progress accelerated and finally generated tangible results that have been translated into practical and better therapeutic strategies. The areas where progress has been more evident are those currently believed to be the key components of IBD pathogenesis, and include the environment, genetics, enteric microbiology, and immune reactivity. Progress in these different areas has been somewhat uneven, yielding a better understanding of the mechanisms behind gut inflammation and tissue injury rather than of specific etiological agents or predisposing factors. However, with the rapidly increasing utilization of novel methodological approaches like genetics, genomics, proteomics, and pharmacogenomics, it is reasonable to anticipate that the etiopathogenesis of IBD will be unveiled in the next couple of decades and more definitive, perhaps disease-modifying, approaches will be uncovered and implemented. [Copyright &y& Elsevier]

Selenium plays important roles in antagonizing the toxicity of methylmercury. The underlying mechanism for the antagonism between Se and MeHg is still not fully understood. The role of gut flora against the toxicity of environmental contaminants is receiving more and more attention. The objective of this study was to investigate the role of Se against MeHg-poisoning in the modulation of gut flora and the decomposition of MeHg. MeHg-poisoned rats were treated with sodium selenite every other day for 90 days. Fecal samples were collected on Day 8, 30, 60 and 90. Gut flora in feces was determined using 16S rRNA gene profiling, and the concentrations of Se and total mercury (THg) were measured by ICP-MS, and the concentration of MeHg was measured by CVAFS. Gut flora at both the ranks of phylum and genus in the MeHg-poisoned rats after Se treatment was modulated towards that in the control group, suggesting the restoration of the profile of gut flora. Increased THg was found in fecal samples after Se treatment on day 30. The percentage of MeHg (of total mercury) in the MeHg-poisoned group was in the range of 81–105% while it was 65–84% in the Se treatment group on different days, suggesting the increased decomposition of MeHg in MeHg-poisoned rats after Se treatment. This study suggests that MeHg poisoning damaged the abundance of gut flora and decreased their capacity for the decomposition of MeHg. After Se treatment, the abundance of gut flora was partially restored and the decomposition and excretion of MeHg was enhanced. These findings suggest that the modulation of gut flora may be one way to promote the health status in MeHg-poisoned rats and possibly in human beings. • Se treatment modulated the diversity and abundance of gut flora in MeHg-poisoned rats. • Se treatment promoted the demethylation of MeHg. • MeHg poisoning damaged teh abuandance of gut flora. [ABSTRACT FROM AUTHOR]

Background & Aims: Rifaximin is used to treat patients with functional gastrointestinal disorders, but little is known about its therapeutic mechanism. We propose that rifaximin modulates the ileal bacterial community, reduces subclinical inflammation of the intestinal mucosa, and improves gut barrier function to reduce visceral hypersensitivity. Methods: We induced visceral hyperalgesia in rats, via chronic water avoidance or repeat restraint stressors, and investigated whether rifaximin altered the gut microbiota, prevented intestinal inflammation, and improved gut barrier function. Quantitative polymerase chain reaction (PCR) and 454 pyrosequencing were used to analyze bacterial 16S ribosomal RNA in ileal contents from the rats. Reverse transcription, immunoblot, and histologic analyses were used to evaluate levels of cytokines, the tight junction protein occludin, and mucosal inflammation, respectively. Intestinal permeability and rectal sensitivity were measured. Results: Water avoidance and repeat restraint stress each led to visceral hyperalgesia, accompanied by mucosal inflammation and impaired mucosal barrier function. Oral rifaximin altered the composition of bacterial communities in the ileum (Lactobacillus species became the most abundant) and prevented mucosal inflammation, impairment to intestinal barrier function, and visceral hyperalgesia in response to chronic stress. Neomycin also changed the composition of the ileal bacterial community (Proteobacteria became the most abundant species). Neomycin did not prevent intestinal inflammation or induction of visceral hyperalgesia induced by water avoidance stress. Conclusions: Rifaximin alters the bacterial population in the ileum of rats, leading to a relative abundance of Lactobacillus. These changes prevent intestinal abnormalities and visceral hyperalgesia in response to chronic psychological stress. [Copyright &y& Elsevier]