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International audience; Persistent Helicobacter pylori (H. pylori) infection is related to 90% of gastric cancers. With bacterial resistance rising and treatment inefficiency affecting 15% of the patients, alternative treatments urge. Chitosan microspheres (ChMics) have been proposed as an H. pylori-binding system. This work evaluates ChMics biocompatibility, mucopenetration and capacity to treat H. pylori infection in mice after oral administration. ChMics of different size (XL, ∼120 µm and XS, ∼40 µm) and degree of acetylation (6% and 16%) were developed and revealed to be able to adhere both human and mouse-adapted H. pylori strains without cytotoxicity towards human gastric cells. Ex vivo studies showed that smaller (XS) microspheres penetrate further within the gastric foveolae, suggesting their ability to reach deeply adherent bacteria. In vivo assays showed 88% reduction of infection when H. pylori-infected mice (C57BL/6) were treated with more mucoadhesive XL6 and XS6 ChMics. Overall, ChMics clearly demonstrate ability to reduce H. pylori gastric infection in mice, with chitosan degree of acetylation being a dominant factor over microspheres' size on H. pylori removal efficiency. These results evidence the strong potential of this strategy as an antibiotic-free approach to fight H. pylori infection, where microspheres are orally administered, bind H. pylori in the stomach, and remove them through the gastrointestinal tract. STATEMENT OF SIGNIFICANCE: Approximately 90% of gastric cancers are caused by the carcinogenic agent Helicobacter pylori, which infects >50% of the world population. Bacterial resistance, reduced antibiotic bioavailability, and the intricate distribution of bacteria in mucus and within gastric foveolae hamper the success of most strategies to fight H. pylori. We demonstrate that an antibiotic-free therapy based on bare chitosan microspheres that bind and remove H. pylori from stomach can achieve 88% reduction of infection from H. pylori-infected mice. Changing size and mucoadhesive properties, microspheres can reach different areas of gastric mucosa: smaller and less mucoadhesive can penetrate deeper into the foveolae. This promising, simple and inexpensive strategy paves the way for a faster bench-to-bedside transition, therefore holding great potential for clinical application.

Helicobacter pylori (H. pylori) gastric infection is considered one of the most common human infections. It occurs in half of the world’s population is the most common cause of adenocarcinoma of the distal stomach [1]. [...]

Gastric cancers are a group of highly aggressive malignancies with a huge disease burden worldwide. Gastric infections, such as helicobacter pylori, can induce the occurrence of gastric cancers. However, the role of gastric infection in gastric cancer development is unclear. Programmed death-ligand 1 (PD-L1, B7-H1) is a member of the B7 family of cell surface ligands, which binds the PD-1 transmembrane receptor and inhibits T-cell activation within cancer tissues. It has been reported that the expression of PD-L1 is inversely related to the prognosis of patients with gastric cancers. Therefore, the regulation of PD-L1 expression in gastric cancers needs to be studied. In the current study, we explored the possible effects of lipopolysaccharide (LPS) on PD-L1 expression in gastric cancer cells. We observed that LPS stimulation could markedly increase PD-L1 expression in gastric cancer cells. Furthermore, we found that nuclear factor-κB (NF-κB) activation was involved in PD-L1 expression in gastric cancer cells exposed to LPS stimulation through p65-binding to the PD-L1 promoter. Taken together, these data indicate that gastric infection might promote the development of gastric cancers thought the LPS-NF-κB-PD-L1 axis.

Helicobacter pylori infection is one of the major risk factors for gastric cancer development. Available antibiotic-based treatments not only fail in around 20% of patients but also have a severe negative impact on the gut microbiota. Recently, we demonstrated that nanostructured lipid carriers (NLC), even without any drug loaded, are bactericidal against H. pylori at low concentrations. This work aims to clarify NLC mode of action and to evaluate if their bactericidal effect is specific to H. pylori without affecting bacteria from microbiota. NLC were produced by hot homogenization followed by ultrasonication method, using Precirol®ATO5 and Miglyol®812 as lipids and Tween®60 as a surfactant. NLC were able to eradicate H. pylori without affecting the other tested bacteria (Lactobacillus, E. coli, S. epidermidis and S. aureus). Bioimaging assays demonstrated that NLC rapidly bind to and cross the H. pylori bacterial membrane, destabilizing and disrupting it, which leads to leakage of the cytoplasmic contents and consequent bacterial death. In an era where efficient alternatives to antibiotics are urgent, NLC are an interesting route to be explored in the quest for new antibiotic-free therapies to fight H. pylori infection.

Nucleotide-binding oligomerization domain 1 (NOD1) is an intracellular innate immune sensor for small molecules derived from bacterial cell components. NOD1 activation by its ligands leads to robust production of pro-inflammatory cytokines and chemokines by innate immune cells, thereby mediating mucosal host defense systems against microbes. Chronic gastric infection due to Helicobacter pylori (H. pylori) causes various upper gastrointestinal diseases, including atrophic gastritis, peptic ulcers, and gastric cancer. It is now generally accepted that detection of H. pylori by NOD1 expressed in gastric epithelial cells plays an indispensable role in mucosal host defense systems against this organism. Recent studies have revealed the molecular mechanism by which NOD1 activation caused by H. pylori infection is involved in the development of chronic gastritis and gastric cancer. In this review, we have discussed and summarized how sensing of H. pylori by NOD1 mediates the prevention of chronic gastritis and gastric cancer.

Background Helicobacter pylori (H. pylori) infection has been associated with gastritis, gastric ulcer, mucosa-associated lymphoid tissue lymphoma and gastric cancer. The prevalence of H. pylori virulence genes have been studied in different populations and from different sources of samples but their prevalence has not been studied in dental plaque in Jordanian people; therefore, the aim of this study was to determine the genotypes of H. pylori isolated from dental plaque samples. Methods Dental plaque samples were collected from 60 Jordanian volunteers. The genotypes of H. pylori virulence genes including the cytotoxin-associated gene A (cagA) and the vacuolating toxin (vacA) were determined using polymerase chain reaction (PCR). Results The cagA gene was detected in 14 (23.3%) samples, while vacA was detected in all volunteers enrolled in this study (100%). The most prevalent vacA alleles were m2 and s1 in 54 (90%) and 55 (91.7%) of volunteers, respectively. Compared to the other combinations including the most virulent vacA genotype s1/m1 which was detected in 11 (18.2%) of volunteers, the most prevalent vacA allelic combinations were s1/m2 and s2/m2 in 56 (93.3%) and 27 (45%) of volunteers, respectively. Conclusions These results indicate a significant carriage of virulent H. pylori strains among Jordanian people in their dental plaques, which increases the possible transmission of these strains among them. In addition, the studying of the genotypic pattern of H. pylori virulence genes in the dental plaque could represent an essential tool for infection prevention and predicting the severity and prognosis of H. pylori gastric infection.

Helicobacter pylori (H. pylori) is a 0.5–1 µm wide, 2–4 µm long, short helical, S-shaped Gram-negative microorganism. It is mostly found in the pyloric region of the stomach and causes chronic gastric infection. It is estimated that these bacteria infect more than half of the world’s population. The mode of transmission and infection of H. pylori is still not known exactly, but the faecal–oral and oral–oral routes via water or food consumption are thought to be a very common cause. In the last three decades, research interest has increased regarding the pathogenicity, microbial activity, genetic predisposition, and clinical treatments to understand the severity of gastric atrophy and gastric cancer caused by H. pylori. Studies have suggested a relationship between H. pylori infection and malabsorption of essential micronutrients, and noted that H. pylori infection may affect the prevalence of malnutrition in some risk groups. On the other hand, dietary factors may play a considerably important role in H. pylori infection, and it has been reported that an adequate and balanced diet, especially high fruit and vegetable consumption and low processed salty food consumption, has a protective effect against the outcomes of H. pylori infection. The present review provides an overview of all aspects of H. pylori infection, such as clinical features, treatment, and nutrition.

BACKGROUND Helicobacter pylori (H. pylori) gastric infection is a main cause of inflammatory changes and gastric cancers. OBJECTIVE The aim of this study was finding the effects of curcumin on oxidative stress and histological changes in chronic gastritis associated with H. pylori. METHODS In a randomized clinical trial, patients were divided into two groups: a standard triple therapy group and triple therapy with curcumin group. Endoscopic and histological examinations were measured for all patients before and after 8 weeks. RESULTS Triple therapy with curcumin treatment group significantly decreased malondialdehyde markers, glutathione peroxides and increased total antioxidant capacity of the gastric mucosa at the end of study compared to baseline and triple regimen groups. In addition, the oxidative damage to DNA was significantly decreased in triple therapy with curcumin group at the end of study compared to baseline and compared to triple therapy (P

Introduction: Helicobacter pylori (H. pylori) is a pathogen which is capable of colonizing the gastric mucosa and is associated with some pathological changes that may lead to dyspeptic manifestations. Recently, H. pylori was found to be present in the oral cavity and there was a growing body of evidence that the organism is linked to some dental diseases such as periodontitis and gingivitis. Materials and Method: In this study, 123 patients were investigated to explore the possible relationship between the presence of oral H. pylori and gastric dyspepsia. Patients were classified into oral disease group (viz. gingivitis and periodontitis) or gastric disease group (viz. gastritis, gastric ulcer, and duodenal ulcer). A third group had neither had oral nor gastric disease. Based on the presence or absence of H. pylori, patients were also classified as having either oral, gastric, or both oral and gastric organism. Some of the patients were neither having oral nor gastric infection. Results: 59 patients showed the presence of H. pylori in the gastro-duodenal area, 7 showed presence of oral H. pylori, whereas 18 patients showed H. pylori in both gastro- duodenal and oral specimens. Differences between groups were not statistically significant. Conclusions: Although there was a suggestion of a clinical and laboratory evidence of an association between the presence of oral H. pylori and the studied gastric diseases, this association was not statistically significant.

BACKGROUND Many studies have reported an association between periodontal infections and some systemic diseases such as respiratory and cardiovascular diseases. Some studies found a direct association between chronic gastritis caused by Helicobacter pylori (HP) infection and poor periodontal health. METHODS In a cross-sectional study from November 2014 to December 2015 in Kerman, the largest province in southeast Iran, patients with dyspepsia who were candidate for diagnostic upper gastrointestinal (GI) endoscopy were included in our study. Decayed, Missing, and Filled Teeth (DMFT) index and Loe plaque index that are two popular indexes in dental epidemiology were used to assess the oral health by a dentist before the upper GI endoscopy. According to the Loe plaque index, score: 0= no plaque, score: 1= a film of plaque attaching to the free gingival border and near area of the tooth, score: 2= moderate reposition of deposits within the gingival pocket, score:3= plenty of soft matter within the gingival pocket±on the tooth and gingival border. Scores ≤1, 2 and 3 equal to good, moderate, and poor oral hygiene, respectively. During upper GI endoscopy a total of six biopsy samples were taken from fundus, body, and antrum. A pathologist reported these samples according to Sidney’s classification into superficial gastritis, atrophic gastritis, intestinal metaplasia, and dysplasia. RESULTS According to Sidney’s classification 77 (89.5%) patients had superficial gastritis, 3 (3.5%) had atrophic gastritis, and 6 (7%) had intestinal metaplasia. HP was found in 80.2% of the gastric mucosal biopsy samples. There were not statistically significant relationship between Sidney’s classification, presence of HP in gastric mucosal biopsies, and hygiene indicators (p>0.05). No relation was found between the DMFT index and superficial gastritis, atrophic gastritis, and intestinal metaplasia (p>0.05). Gastric infection with HP was found in 70%, 75%, and 100% of patients with mild, moderate, and sever DMFT index, respectively. CONCLUSION Our study showed that there might be a relation between poor oral hygiene and gastric precancerous lesions. In addition, HP infection in gastric histopathology might be associated with periodontal disease.

Background/Aim. Helicobacter (H.) pylori is a widespread bacterium and its involvement in pathogenesis of gastric diseases is well-known. However, H. pylori role in etiology of other histologically similar conditions, especially recurrent aphthous stomatitis (RAS) is still controversial. Research regarding H. pylori and its association with RAS, as well as the treatment options were always conducted on patients with diagnosed gastric problems. The aim of this study was to determine whether H. pylori is present in the oral cavity of patients suffering from RAS but without any symptoms or medical history of gastric disease. Methods. A total of 15 patients with RAS participated in the study. None of the participants suffered from any gastrointestinal disorders. Two dental plaque samples from each participant were collected. The first was analyzed using rapid urease test and the second one was put in transport medium and sent for cultivation. The sensitivity of H. pylori to antibiotics was established using disk diffusion method of sensitivity testing for every patient individually and adequate therapy was prescribed. Results. Before the treatment the mean annual recurrence rate of RAS was 8.1 ± 2.1, with the average number of lesions being 3.9 ± 1.9. During the 12-month observation period after the eradication therapy, none of the patients reported recurrence of aphthous lesions. The treatment was successful in all cases. Conclusion. This study shows that RAS can be effectively treated by successful eradication of oral H. pylori, and that RAS could be possibly considered as an early warning sign of potential gastric infection by H. pilory., Uvod/Cilj. Helicobacter (H.) pylori je široko rasprostanjena bakterija i njen uticaj na nastanak gastričkih oboljenja vrlo dobro je dokumentovan. Međutim, uloga H. pylori u patogenezi histološki sličnih oboljenja, posebno rekurentnog aftoznog stomatitisa (RAS), nije dovoljno istražena. Dosadašnje studije, u kojima je ispitivana veza između H. pylori i RAS, kao i moguće terapijske opcije, bile su usmerene ka bolesnicima sa prethodno dijagnostikovanim gastričkim smetnjama. Cilj ovog istraživanja bio je da se utvrdi da li je H. pylori prisutan u usnoj duplji i kod bolesnika bez simptoma i istorije gastričkih oboljenja koji pate od RAS. Metode. U studiji je učestvovalo 15 bolesnika koji pate od RAS. Bolesnici nisu imali smetnje vezane za gornji deo digestivnog trakta. Po dva uzorka dentalnog plaka prikupljena su od svakog bolesnika. Jedan plak je ispitivan uz pomoć brzog ureaza testa, dok je drugi stavljen u transportni medijum i poslat na kultivaciju. Osetljivost H. pylori na antibiotike određivana je uz pomoć antibiograma za svakog bolesnika posebno i, u skladu sa rezultatima, prepisivana je odgovarajuća terapija. Rezultati. Pre lečenja prosečan broj epizoda RAS tokom godine iznosio je 8,1 ± 2,1, sa prosečno 3,9 ± 1,9 aftoznih lezija. Tokom 12-mesečnog perioda nakon eradikacione terapije, ni kod jednog bolesnika nije došlo do ponovne pojave afti. Terapija je bila uspešna kod svih bolesnika. Zaključak. Rezultati ovog istraživanja pokazuju da se RAS može uspešno lečiti eradikacijom H. pylori i da se sama pojava RAS može posmatrati kao rano upozorenje na moguću gastričku infekciju.

Helicobacter pylori causes chronic gastric infection that can lead to peptic ulcers and is an identified risk factor for gastric cancer development. Although much effort has been put into the development of a Helicobacter pylori vaccine over the last three decades, none has yet reached clinical application. Specific challenges pertaining to effective H. pylori vaccine development include the lack of proven vaccine-effective antigens and safe mucosal adjuvants to enhance local immune responses as well as the lack of accepted correlates of protection. Herein, we demonstrate that prophylactic intragastric immunisation with a whole-cell killed H. pylori antigen administered together with the non-toxic oral adjuvant α-galactosylceramide (α-GalCer) induced effective immune protection against H. pylori infection in mice, which was of similar magnitude as when using the “gold standard” cholera toxin as adjuvant. We further describe that this α-GalCer-adjuvanted vaccine formulation elicited strong intestinal and systemic Th1 responses as well as significant antigen-specific mucosal and systemic antibody responses. Finally, we report that the protective intestinal Th1 responses induced by α-GalCer are dependent on CD1d, IL-1R as well as IL-17R signalling. In summary, our results show that α-GalCer is a promising adjuvant for inclusion in an oral vaccine against H. pylori infection., Helicobacter pylori: prophylactic intragastric immunisation with oral adjuvant Infection by Helicobacter pylori is highly prevalent in humans and can lead to chronic inflammation and gastric cancer, but to date no effective vaccine has been approved for clinical use owing to the lack of appropriate antigens and of safe mucosal adjuvants that can produce protective and durable immunity to the bacterium. Sukanya Raghavan, Ed Lavelle and colleagues now show that prophylactic intragastric administration of an inactivated whole-cell H. pylori preparation, together with the oral adjuvant α-galactosylceramide, reduced H. pylori infection in mice by eliciting a protective mucosal and systemic TH1 response. The immunisation triggered antigen-specific antibodies and interferon-γ that prevented effective colonisation of H. pylori after challenge in a process dependent on the CD1d, IL-1 receptor and IL-17 receptor pathways. The reported enhanced immune response to this orally adjuvanted vaccine formulation paves the way for further studies of its safety and efficacy.

Macrorhabdus ornithogaster is an opportunistic yeast that colonizes the gastric mucosa of many avian species. Until now, no studies have focused on the influence of a gastric infection on the balance of the intestinal microbiota of birds. In this study, 44 faecal samples from individual canaries, with and without M. ornithogaster infection, were analysed. The detection of the yeast was evaluated by 18S rRNA PCR. In order to evaluate the impact of the Macrorhabdus infection on the bacterial communities, culture-independent methods, by the use of amplicon-based sequencing as well as 16S rRNA-DGGE, were adopted. The different health status of animals affected the relative abundance of the main OTUs, with a greater diversification of the gut microbiota in healthy animals compared to the infected. In particular, Lactococcus, Pseudomonas, Acinetobacter, Lachnospiraceae, Propionibacterium and Weissella were found to be characteristic of uninfected animals (FDR 0.05), while Lactobacillus and Candidatus Arthromitus were characteristic of infected animals (FDR 0.05). Both these taxa have been reported as immunostimulatory, involved in immunological disorders. In infected animals the inferred metagenome assessed by PICRUST clearly showed a positive correlation between the presence of M. ornithogaster and KEGG genes related to ether lipid metabolism, already reported to be immunostimulatory by activation of macrophages and to play a pathophysiological role in several immunological disorders. Finally, our results show an interaction between infection of the digestive tract and intestinal microbiota of pet birds and provide insight into the changing of the complex enteric bacterial community. HIGHLIGHTS Macrorabdus ornithogaster is a gastric yeast that colonizes a wide range of birds. Differences were found between infected and healthy animals in gut microbiota. Candidatus Arthromitus was closely associated with infected birds. M. ornithogaster can affect intestinal microbiota composition of canaries.

Some research has suggested that dental plaque and saliva could be reservoirs of Helicobacter pylori ( H. pylori ) and be capable of infecting or re-infecting the gastric mucosa after eradication, with certain studies showing a significant association between PD and gastric infection by this bacterium. An electronic search was performed in PubMed, EMBASE, and Web of Science databases with the terms " Helicobacter pylori AND periodontal diseases"; " Helicobacter pylori AND gingivitis"; " Helicobacter pylori AND chronic periodontitis"; " Helicobacter pylori AND periodontitis"; " Helicobacter pylori AND dental plaque", to identify articles up to September 2021. The Newcastle-Ottawa scale was used to assess study quality. A meta-analysis was performed using RevMan 2020 (Cochane Collaboration) software. A total of 1,315 studies were identified and 12 were included, analyzing 226,086 patients with mean age between 10.5 and 63.4 years. The prevalence of H. pylori in the oral cavity ranged from 5.4 to 83.3%. A random-effects model was used to analyze the presence of H. pylori and subgroups were made according to the method of evaluation (PCR or RUT). Statistical significance was found in the overall analysis ( p = 0.01). There is no clear evidence that H. pylori present in oral bacterial plaque causes gastric infection and vice versa., Systematic Review Registration: www.INPLASY.COM, identifier: INPLASY2021100097., Competing Interests: The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest., (Copyright © 2022 López-Valverde, Macedo de Sousa, López-Valverde, Suárez, Rodríguez and Aragoneses.)

Non-Helicobacter pylori-Helicobacters including H. suis, H. heilmanniisensu stricto and H. felis comprise a group of bacteria that may inhabit the stomach of humans and animals. Human gastric infection has been associated with gastritis, ulcer, MALT lymphoma and cancer. Although the fastidious nature of these organisms has hampered their research, recent advancements in in vitro cultivation and recent reports on in vivo models and prevalence studies in humans suggest this group of bacteria to be of more clinical significance than earlier believed. The present review discusses their history, microbiology and relevance to human health.

Background: Helicobacter pylori (H. pylori) is considered as one of the most prevalent gastric infections which cause chronic gastritis and predispose to cancer stomach. So, diagnosis and eradication should be rapid to decrease the risk of gastric cancer. Aim of the study: To evaluate the role of rapid urease test (RUT) and faecal antigen test (FAT) added to serological test for rapid diagnosis of active H. pylori infection. Patients and methods: 270 patients with dyspepsia and positive serology for H. pylori infection were included. Two antral and two corporal gastric biopsies were taken for RUT and Histopathological examination. Fresh stool samples were obtained from all patients for FAT. Results: The mean age of the studied patients was 45 ± 25. H. pylori infection was found in 256 (94.8%) of the included patients: 236 (92.18%) with positive all tests, 5 (1.95%) with positive both RUT and FAT, 8 (3.12%) with positive both histology and RUT and 7 (2.73%) with positive histology and FAT. The sensitivity, specificity and positive predictive values for RUT were as follows: 97.27%, 85.71% and 99.20% respectively and 96.88%, 85.71% and 99.20% respectively for FAT. Conclusions: RUT or FAT in patients with positive serological test could be used for rapid diagnosis of active H. pylori infection with good sensitivity and specificity without waiting for the results of histology or culture.

Helicobacter pylori affect around 50% of the population worldwide. More importantly, the gastric infection induced by this bacterium is deemed to be associated with the progression of distal gastric carcinoma and gastric mucosal lymphoma in the human. H. pylori infection and its prevalent genotype significantly differ across various geographical regions. Based on numerous virulence factors, H. pylori can target different cellular proteins to modulate the variety of inflammatory responses and initiate numerous “hits” on the gastric mucosa. Such reactions lead to serious complications, including gastritis and peptic ulceration, gastric cancer and gastric mucosa-associated lymphoid structure lymphoma. Therefore, H. pylori have been considered as the type I carcinogen by the Global Firm for Research on Cancer. During the two past decades, different reports revealed that H. pylori possess oncogenic potentials in the gastric mucosa through a complicated interplay between the bacterial factors, various facets, and the environmental factors. Accordingly, numerous signaling pathways could be triggered in the development of gastrointestinal diseases (e.g., gastric cancer). Therefore, the main strategy for the treatment of gastric cancer is controlling the disease far before its onset using preventive/curative vaccination. Increasing the efficiency of vaccines may be achieved by new trials of vaccine modalities, which is used to optimize the cellular immunity. Taken all, H. pylori infection may impose severe complications, for resolving of which extensive researches are essential in terms of immune responses to H. pylori. We envision that H. pylori-mediated diseases can be controlled by advanced vaccines and immunotherapies.

Aim This study was aimed to identify the presence of Helicobacter pylori (H. pylori) genes in oral mucosa and find out their relationship between oral H. pylori infection and gastric complications. Methods This study is a case control study consists of 567 subjects with periodontal infection (278 gastric complication cases and 289 controls normal gastric intestinal mucosa) with age range of 20–80 years. Oral health status was recorded by calculating oral hygiene index (OHI), probing depths (PD) and clinical attachment loss (CAL). Each participant provided gastric biopsy and plaque samples which were subjected to H. pylori detection. Polymerase chain reaction (PCR) with different primers specifically β globulin, 16SrRNA, babA, cagA, ureA, ureC and vacA gene was performed which were then analyzed using gel electrophoresis. Results No significant differences (χ2 = 11.873, p value > 0.05) were observed between oral H. pylori and gastric infections/complications. However, H. pylori increase the risk of developing gastro-esophageal reflux grade II (OR = 1.458, 95%CI = 0.659–3.226), normal upper GIT mucosa with lax esophageal sphincters (OR = 1.215, 95%CI = 0.285–5.181) and duodenal ulcer/duodenitis (OR = 2.187, 95%CI = 0.225–21.278). This study also showed a significant increased risk of gastritis with babA gene. Conclusion Oral pathogenic H. pylori genes may enhance the severity of the gastric infection.

Background: Helicobacter pylori infection is a major global gastric infection and has been associated with changes in haematological parameters. Objectives: The present study aimed at establishing the effect of H. pylori infection on haematological parameters. Methods: We conducted a case-control study among 98 patients and 62 controls in Kosti teaching hospital in Sudan from July 2014 to July 2015. All patients and controls were investigated for complete blood count, peripheral blood picture, and Helicobacter pylori infection. Data were analysed using SPSS Version 23 at 95% confident interval. Results: There was a significant effect of H. Pylori infection on all haematological parameters (p ≤ 0.001), except for MCHC, WBCs, and total differential (p ≥ 0.001), at the rate of 89.80%, infection was recorded in patients with gastritis. However, after one month follow- up, the Hb, PCV, MCV Retic, and platelet count for GIa were found to be not significant (p ≥ 0.001) for all; 12.11 ± 1.11 g/dL, 40.33 ± 3.09 %, 81.36 ± 3.5 fL and 1.38 ± 0.84 %, 233700.0000 ± 34947.7400 cmm3, respectively. On the other hand, GIb, Hb, PCV, MCV, Retic and platelet counts were reported to be significant (p ≤ 0.001), for all; 10.33 ± 1.82 g/dL, 33.99 ± 3.48%, 111.01 ± 7.89 fL, 3.20 ± 1.24 % and 112895.6000 ± 41043.0500 cmm3. In the GII, all were found to be significant (p < 0.001), 8.58 ± 1.93 g/dL, 30.86 ± 3.10 %, 60.13 ± 4.44 fL 4.53 ± 1.84%, 317818.2000 ± 91442.7600 cmm3, except for the retic and platelet count (p ≥ 0.001). Conclusions: There was a significant effect of H. pylori infection on haematological parameters. The complete blood count and peripheral blood picture revealed that group Ia, group Ib, and group II were normocytic anemia, macrocytic anemia, and microcytic anemia, respectively.

The minimum inhibitory concentration of bambermycin on three porcine Helicobacter suis strains was shown to be 8 μg/mL. The effect of in-feed medication with this antibiotic on the course of a gastric infection with one of these strains, the host response and the gastric microbiota was determined in mice, as all of these parameters may be involved in gastric pathology. In H. suis infected mice which were not treated with bambermycin, an increased number of infiltrating B-cells, T-cells and macrophages in combination with a Th2 response was demonstrated, as well as a decreased parietal cell mass. Compared to this non-treated, infected group, in H. suis infected mice medicated with bambermycin, gastric H. suis colonization was not altered, but a decreased number of infiltrating T-cells, B-cells and macrophages as well as downregulated expressions of IL-1β, IL-8M, IL-10 and IFN-γ were demonstrated and the parietal cell mass was not affected. In bambermycin treated mice that were not infected with H. suis, the number of infiltrating T-cells and expression of IL-1β were lower than in non-infected mice that did not receive bambermycin. Gastric microbiota analysis indicated that the relative abundance of bacteria that might exert unfavorable effects on the host was decreased during bambermycin supplementation. In conclusion, bambermycin did not affect H. suis colonization, but decreased gastric inflammation and inhibited the effects of a H. suis infection on parietal cell loss. Not only direct interaction of H. suis with parietal cells, but also inflammation may play a role in death of these gastric acid producing cells. Electronic supplementary material The online version of this article (10.1186/s13567-018-0530-1) contains supplementary material, which is available to authorized users.

Minor infections cause big problems Pathogenic infection has been implicated in the chronic inflammation seen in inflammatory bowel diseases (IBDs) such as ulcerative colitis and Crohn's disease. Yang et al. show that recurrent, low-level, and fully resolving Salmonella enterica Typhimurium (ST) infections can precipitate severe colonic inflammation in mice. ST-induced TLR4 activation resulted in increased neuraminidase 3 (Neu3) production and activity in the duodenum. This led to intestinal alkaline phosphatase (IAP) desialylation and degradation. IAP deficiency caused a marked increase in commensal bacteria-generated lipopolysaccharide-phosphate in the colon, provoking inflammation. Treatment with calf IAP or the antiviral drug zanamivir (which inhibits Neu3 activity) prevented this inflammatory cascade. This pathway may serve as an effective target for future human IBD therapies. Science , this issue p. eaao5610

Background The oral cavity can be an extra-gastric reservoir for Helicobacter pylori (H.pylori). This can play a role in the pathogenesis of halitosis, glossitis, recurrent aphthous stomatitis, and dental caries. The present study was conducted to detect the presence of H.pylori within the dental biofilm and in saliva samples collected from children suffering from dyspepsia and children without any gastrointestinal complaints. Associations with gastric infection, halitosis, and some oral parameters were also evaluated. Methods Seventy children (aged between 5–16) with dyspepsia were selected for the study group and control group composed of 30 healthy children without dyspepsia were also included in the study. After detailed oral and clinical examinations for oral parameters, saliva, and supragingival dental biofilm samples were collected for 16S rRNA and 23S rRNA genes detection by real-time polymerase chain reaction (RT-PCR). The presence of gastric H.pylori was evaluated in endoscopic biopsy specimens histopathologically. Halitosis was evaluated by benzoyl-DL-arginine-naphthylamid (BANA) test. Salivary S.mutans and Lactobacilli sp. counts were also carried out by commercial kits. Results H.pylori was histopathologically detected amongst 83% of the children with the dyspeptic condition. The detection rate of this bacteria in dental biofilm and saliva samples and halitosis were found relatively higher in the dyspeptic children rather than the control group (p 0.05). In the gastric H.pylori positive group with dyspepsia, DMFT/S and dmft/s numbers and plaque indices were found higher than the control group (p 0.05). Comparing to those with negative for both genes, in children whose dental biofilm and saliva samples were positive for both 16S rRNA and 23S rRNA genes, significantly higher results for halitosis, and DMFS numbers and significantly lower results for dmfs numbers and pH values were found (p

At present, biopsy specimens, cancer cell lines and tissues obtained by gastric surgery are used in the study and analysis of gastric cancer, including the molecular mechanisms and proteomics. However, fibroblasts and other tissue components may interfere with these techniques. Therefore, the present study aimed to develop a procedure for the isolation of viable human gastric epithelial cells from gastric surgical tissues. A method was developed to culture human gastric epithelial cells using fresh, surgically excised tissues and was evaluated using immunocytochemistry, periodic acid-Schiff (PAS) staining and cell viability assays. Low cell growth was observed surrounding the gastric tissue on the seventh day of tissue explant culture. Cell growth subsequently increased, and at 12 days post-explant a high number of pure epithelial cells were detected. The gastric cancer cells exhibited rapid growth with a doubling time of 13-52 h, as compared to normal cells, which had a doubling time of 20-53 h. Immunocytochemical analyses of primary gastric cells revealed positive staining for cytokeratin 18 and 19, which indicated that the culture was comprised of pure epithelial cells and contained no fibroblasts. Furthermore, PAS staining demonstrated that the cultured gastric cells produced neutral mucin. Granulin and carbohydrate antigen 724 staining confirmed the purity of gastric cancer and normal cells in culture. This method of cell culture indicated that the gastric cells in primary culture consisted of mucin-secreting gastric epithelial cells, which may be useful for the study of gastric infection with Helicobacter pylori and gastric cancer.

Background Helicobacter pylori infection has been consistently associated with lack of access to clean water and proper sanitation, but no studies have demonstrated that the transmission of H. pylori can occur from drinking contaminated water. In this study, we used a laboratory mouse model to test whether waterborne H. pylori could cause gastric infection. Materials and Methods Groups of immunocompetent C57/BL6 Helicobacter-free mice were exposed to static concentrations (1.29 × 105, 106, 107, 108, and 109 CFU/L) of H. pylori in their drinking water for 4 weeks. One group of Helicobacter-free mice was exposed to uncontaminated water as a negative control. H. pylori morphology changes in water were examined using microscopy Live/Dead staining. Following exposure, H. pylori infection and inflammation status in the stomach were evaluated using quantitative culture, PCR, the rapid urease test, and histology. Results None of the mice in the negative control or 105 groups were infected. One of 20 cages (one of 40 mice) of the 106 group, three of 19 cages (four of 38 mice) of the 107 CFU/L group, 19 of 20 cages (33 of 40 mice) of the 108 group, and 20 of 20 cages (39 of 40 mice) of the 109 CFU/L group were infected. Infected mice had significantly higher gastric inflammation than uninfected mice (27.86% higher inflammation, p

Helicobacter pylori is considered to be responsible for the most common gastric infections in humans worldwide. In animals, other Helicobacter species are linked to gastritis with and without the presence of ulcers in their respective hosts. Moreover, gastric ulcers have been reported for decades in wild and captive dolphins. Clinical signs include lack of appetite, anorexia, abdominal tenderness, depression, and occasional unresponsiveness. In this study, serum and stool of nine bottlenose dolphins from Loro Parque collection Tenerife, Spain were examined for the presence of Helicobacter spp. The aim of our study was to evaluate the use of two commercially available kits for the detection of H. pylori in humans: a stool antigen immunoassay (Letitest H. pylori CARD) and a Western blot assay (EUROLINE-WB H. pylori) that were adapted to identify specific Helicobacter spp. antibodies in the tested Loro Parque bottlenose dolphin collection. The utility of these diagnostic kits for their application in dolphins is demonstrated, and their use in the future for the diagnosis of Helicobacter spp. in both wild and captive dolphins is proposed in this study.

A 64-year-old man presented with epigastralgia and nausea after an acute exacerbation of chronic pancreatitis. Abdominal computed tomography revealed remarkable thickening of the gastric wall and intramural hypodense areas. Esophagogastroduodenoscopy showed a large gastric ulcer surrounded by an edematous mucosa and mucopus. The results of a culture from a biopsy of the lesion indicated phlegmonous gastritis. The patient was successfully treated with an antibiotic without gastrectomy.

Helicobacter pylori is a major risk factor for peptic ulcer, but studies on the role of H. pylori infection in gastric pathology are limited due to lack of convenient models resembling H. pylori infection in humans. We studied the effects of inoculation of conventional BALB/c mice with a toxigenic (cytotoxin associated gene A (cagA)+ and vacuolating cytotoxin gene A (vacA+) H. pylori strain on the course of healing of gastric ulcers. Following inoculation of toxigenic H. pylori or vehicle, gastric ulcers were produced in mice, which were then killed either at day 0 or after 2, 4, 7, 14 or 28 days and ulcer area and gastric blood flow (GBF) were determined. Gastric secretions from mice with chronic gastric fistulae were studied before and after inoculation with toxigenic H. pylori or vehicle (saline). The area (7 mm2 ) of ulcers in control mice decreased gradually and disappeared almost completely after 14 or 28 days. The ulcers in H. pylori-infected mice were present at all test days, showing a larger area than in vehicle control animals. The GBF in control mice rose gradually with decreasing ulcer size, being significantly higher at the ulcer margin than the ulcer crater. In contrast, the GBF in H. pylori-infected mice was significantly lower at the ulcer area than that in the vehicle controls but, again, the GBF at the ulcer margin was always higher than at the ulcer crater. Gastric acid output was reduced by more than 50% immediately after H. pylori inoculation and was accompanied by a significant increase in plasma gastrin release and a fall in gastric luminal somatostatin content. These secretory changes persisted at all test days. Oedema/congestion of surface epithelium appeared after 7 days and mucosal inflammatory infiltration appeared after 14 days, to further increase after 28 days, upon the induction of ulcer. Plasma interleukin (IL)-Is and IL-12 were significantly elevated above the initial values compared with controls. Conventional mice with gastric ulcers can be successfully infected with an H. pylori strain expressing cagA and vacA cytotoxin and this infection markedly delays healing of the ulcers, probably due to the fall in GBF in the ulcer area, mucosal inflammation, cytokine release and impairment of the gastrin-somatostatin link.

Emerging evidence shows that the human microbiota plays a larger role in disease progression and health than previously anticipated. Helicobacter pylori , the causative agent of gastric cancer and duodenal and gastric ulcers, was early associated with gastric disease, but it has also been proposed that the accompanying microbiota in Helicobacter pylori -infected individuals might affect disease progression and gastric cancer development. In this study, the composition of the transcriptionally active microbial community and H. pylori gene expression were determined using metatranscriptomic RNA sequencing of stomach biopsy specimens from individuals with different H. pylori infection statuses and premalignant tissue changes. The results show that H. pylori completely dominates the microbiota not only in infected individuals but also in most individuals classified as H. pylori uninfected using conventional methods. Furthermore, H. pylori abundance is positively correlated with the presence of Campylobacter , Deinococcus , and Sulfurospirillum . Finally, we quantified the expression of a large number of Helicobacter pylori genes and found high expression of genes involved in pH regulation and nickel transport. Our study is the first to dissect the viable microbiota of the human stomach by metatranscriptomic analysis, and it shows that metatranscriptomic analysis of the gastric microbiota is feasible and can provide new insights into how bacteria respond in vivo to variations in the stomach microenvironment and at different stages of disease progression.

Three decades have passed since Warren and Marshall described the successful isolation and culture of Helicobacter pylori, the Gram-negative bacterium that colonizes the stomach of half the human population worldwide. Although it is documented that H. pylori infection is implicated in a range of disorders of the upper gastrointestinal tract, as well as associated organs, many aspects relating to host colonization, successful persistence, and the pathophysiological mechanisms of this bacteria still remain controversial and are constantly being explored. Unceasing efforts to decipher the pathophysiology of H. pylori infection have illuminated the crucially important contribution of multifarious bacterial factors for H. pylori pathogenesis, in particular the cag pathogenicity island (PAI), the effector protein CagA, and the vacuolating cytotoxin VacA. In addition, recent studies have provided insight into the importance of the gastrointestinal microbiota on the cumulative pathophysiology associated with H. pylori infection. This review focuses on the key findings of publications related to the pathogenesis of H. pylori infection published during the last year, with an emphasis on factors affecting colonization efficiency, cagPAI, CagA, VacA, and gastrointestinal microbiota.

Peptic ulcer is a lesion in the mucosa of the digestive tract affecting many people all around the world. Recent investigations have indicated that produced inflammatory cytokines such as TNF-α and IL-1β in response to gastric infection by Helicobacter pylori play an important role in the development of peptic ulcer. With regard to the significance of these cytokines in peptic ulcer development and the high prevalence of this disease in the developing countries, this study aimed to investigate the association of TNF-α and IL-1β with peptic ulcer in the presence of H. pylori. This case-control study enrolled 61 patients with peptic ulcer disease (PUD) as cases and 59 people without peptic ulcer (NPUD) as controls. Blood samples and endoscopic biopsies were collected. H. pylori infection was confirmed by using rapid urease test (RUT), specific IgG measurement and histopathological examination. Then, IL-1β and TNF-α levels were evaluated using enzyme linked immunosorbent assay (ELISA). The seropositivity of H. pylori was 62.5% in the studied population, while by considering RUT and histopathological examination along with specific-IgG antibody, H. pylori infection decreased to 56.7%. In addition, H. pylori infection was significantly (OR = 0.37; 95% CI = 0.17–0.82; P = .02) associated with peptic ulcer development. The TNF-α level in PUD and infected H. pylori subjects was significantly higher than that of control and un-infected H. pylori individuals. However, no significant difference of IL1β level was observed between PUD and control groups as well as between H. pylori infected and un-infected individuals. Interestingly, IL-1β level in PUD patients without H. pylori infection was significantly higher than infected ones. Moreover, a significant correlation between specific-IgG antibody with TNF-α level was observed. Taken together, our results showed that increased level of TNF-α could probably play pivotal role in pathogenesis of peptic ulcer in the presence of H. pylori infection. These findings also highlighted the importance of IL-1β in the absence of H. pylori infection in peptic ulcer development.

SummaryBackground Gastric infection with Helicobacter pylori (Hp) can lead to chronic inactive gastritis, atrophy and intestinal metaplasia. Aims To investigate in a cross-sectional study these changes among different socioeconomic and ethnic groups within the USA. Methods We used the Miraca Life Sciences database, an electronic depository of clinicopathological records from patients distributed throughout the USA, to extract data from 487 587 patients who underwent oesophago-gastro-duodenoscopy with biopsy between 1/2008 and 12/2014. We then classified patients into ethnic and socioeconomic categories using previously validated algorithms, as well as ZIP code-based information derived from the 2011-2012 US Census. Results The prevalence of Hp increased significantly until the age-group 40-49, before it leveled off and started a gradual decrease. The prevalence of chronic inactive gastritis, atrophy, and intestinal metaplasia increased significantly with age. The prevalence of Hp, chronic inactive gastritis, intestinal metaplasia, and atrophy decreased significantly with the percentage of Whites per ZIP code. The prevalence of all four diagnoses also decreased significantly with rising levels of income or college education. Hp, chronic inactive gastritis, atrophy and intestinal metaplasia were more common among Hispanics and the influence of income or college education less pronounced than in the entire population. Hp, chronic inactive gastritis, atrophy, and intestinal metaplasia were also more common among East-Asians, Hp and atrophy decreasing with rising income but remaining unaffected by levels of college education. Conclusion Ethnicity and socioeconomic factors influence the occurrence of Hp gastritis, and its progression to chronic inactive gastritis, atrophy or intestinal metaplasia.

Helicobacter pylori (Hp) has a worldwide distribution showing its higher prevalence of infection in developing countries. Toll-like receptors (TLRs) and C-type lectin receptors (CLRs) are proteins that recognize pathogen-associated molecular patterns (PAMPs) and initiate an innate immune response by promoting growth and differentiation of specialized hematopoietic cells for host defense. Gastric infections led by Hp induce a Th-1 cellular immune response, regulated mainly by the expression of IFN-γ. In this retrospective case-control study, we evaluated the TLR1 1805T/G, TLR2 2029C/T, TLR4 896A/G, CD209 -336A/G and IFNGR1 -56C/T polymorphisms and their relationship with susceptibility to Hp infection. TLR1 1805T/G showed statistical differences when the control (Hp-) and infected (Hp+) groups (P = 0.041*) were compared; the TLR1 1805G allele had a protective effect towards infection (OR = 0.1; 95% CI = 0.01-0.88, P = 0.033*). Similarly, the IFNGR1 -56C/T polymorphism showed statistical differences between Hp+ and Hp- (P = 0.018*), and the IFNGR1 -56TT genotype exhibited significant risk to Hp infection (OR = 2.9, 95% CI = 1.27-6.54, P = 0.018*). In conclusion, the pro-inflammatory TLR1 1805T and IFNGR1 -56T alleles are related with susceptibility to Hp infection in Ecuadorian individuals. The presence of these polymorphisms in individuals with chronic infection increases the risk of cellular damage and diminishes the cellular immune response efficiency towards colonizing agents.

UNLABELLED Aloe barbadensis Miller (Aloe vera) is a herbal remedy widely used for a variety of illnesses; A. vera leaf extracts have been promoted for detoxification, cure constipation, help flush out toxins and wastes from the body, promote digestion and are used in the treatment of peptic ulcer for cytoprotective action. The aim of this study was to evaluate the antibacterial activity of A. vera inner gel against both susceptible and resistant Helicobacter pylori strains isolated in Abruzzo region, Italy. The inner gel of leaves of a 5-year-old plant of A. vera was extracted, homogenized and tested from 800 to 1.56 mg ml(-1) against 14 clinical strains and one reference strain of H. pylori using the broth microdilution methodology. Furthermore, the sample of A. vera was investigated for the chemical fingerprint of anthraquinones. The inhibitory concentrations of A. vera inner gel were similar to the bactericidal ones, with values ranging from 6.25 to 800 mg ml(-1) . Fifty per cent of the detected strains, independently of their susceptibility profile, were inhibited in their growth at 100 mg ml(-1) . Aloe vera inner gel expresses antibacterial properties against H. pylori and, therefore, in combination with antibiotics, could represent a novel strategy for the treatment of the infection of H. pylori, especially in cases of multiresistance. SIGNIFICANCE AND IMPACT OF THE STUDY The study demonstrates that the Aloe vera inner gel expresses antibacterial properties against both susceptible and resistant Helicobacter pylori strains. These findings may impact on the antimicrobial resistance phenomenon of H. pylori, proposing the A. vera inner gel as a novel effective natural agent for combination with antibiotics for the treatment of H. pylori gastric infection.

Background. Several studies were reported on the prevalence, and relationship between the existence of Helicobacter pylori (H. pylori) in oral cavity and in stomach of patients. The purpose of this study was to systematically review the existing literature on the presence of H. pylori in the oral cavity and its link to gastric infection, the existence of coinfection, and the impact of anti-H. pylori therapy on the dental plaque and vice versa. Method. Two authors independently searched the Medline, EMBASE, Cochrane Library, Web of Science, Google Scholar, and Scopus databases for relevant studies. The articles were analyzed critically and all qualified studies were included. The search was carried out by using a combined text and the MeSH search strategies: using the key words Helicobacter, Helicobacter pylori, and H. pylori in combination with dental plaque, periodontitis, and oral hygiene. Results. The data was presented in 8 tables and each topic separately discussed. Conclusion. Based on the systematic review of the available literature on H. pylori infection and its presence in the oral cavity, it can be concluded that dental plaque can act as a reservoir, and proper oral hygiene maintenance is essential to prevent reinfection. Due to the diversified methods and population groups involved in the available literature, no concrete evidence can be laid down. Further studies are necessary to establish the role of H. pylori in the oral cavity and its eradication on preventing the gastroduodenal infection.

Cronkhite-Canada syndrome is a rare protein-losing enteropathy, classically characterized by ectodermal changes and gastrointestinal polyposis. The etiology remains obscure but immune dysregulation may be important. The diagnosis of Cronkhite-Canada syndrome in the upper gastrointestinal tract is challenging, frequently resulting in delayed patient management. In this study, we described the initial clinical presentations, upper gastrointestinal endoscopic appearances, clinical follow-up, and histologic diagnoses in 7 patients who were subsequently diagnosed with Cronkhite-Canada syndrome. Histology slides were reviewed, and IgG4 immunohistochemical analysis was performed. The most common initial endoscopic impressions were antral malignancy and gastric infection, but gastroduodenal polyposis was not described. On histologic review, the main findings in the gastric mucosa were a prominent mucosal edema, a mixed inflammatory infiltrate rich in eosinophils, and architectural changes with gland dilatation and withering. In the duodenal mucosa, total or subtotal duodenal villous atrophy, inflammation, crypt distortion, and increased apoptotic bodies were the most common features. Three patients died of the disease, and 4 patients were asymptomatic at a mean follow-up of 3.5 years. No intestinal malignancy had been diagnosed. In 2 patients foci of dysplasia in colonic polyps were identified. In only 1 patient, a significant increase in IgG4-positive plasma cells was observed in a colonic polyp. In summary, we found that patients with Cronkhite-Canada syndrome have histologic features commonly found in other immune disorders of the gastrointestinal tract that may help in establishing the diagnosis and further supports the hypothesis that Cronkhite-Canada syndrome may represent an immune dysregulation syndrome, different from IgG4-related disease.

Helicobacter Pylori (HP) is a Gram-negative, spiral-shaped, motile micro-organism that infects approximately half of the world population and the prevalence of asymptomatic infected patients appears to be age-related (1). The human is its reservoir and the transmission of this microorganism involves oral‑oral and fecal‑oral routes. The infection takes place usually in childhood, within one’s own family (between parents and children or between siblings) (2). Gastric infection by HP is actually considered to be the most relevant cause of chronic gastritis and peptic ulcer disease (PUD). It is also associated with an increased risk of mucosa associated lymphoid tissue (MALT) lymphoma and gastric cancer (3). Selection of the best drug regimens for effective eradication of HP infection is challenging. Some recent studies have suggested that the effectiveness, compliance and side-effects of quadruple regimen containing a gastric acid inhibitor, a bismuth compound and two antibiotics might be comparable with proton pump inhibitors (PPI) -based triple therapy when administered as first-line treatment for HP infection (4-6). However, in other studies showed superiority of quadruple therapy (7). Antibiotic resistance due to frequent and uncontrolled administration and high prevalence of antibiotic side effects are the most common causes of treatment failure. To increase eradication rate, as defined in the Maastricht IV report (8), several clinical trials have been initiated involving extended treatment duration, use of new antibiotics or the addition of probiotics or other drugs regimens (9). In the Maastricht Consensus Report, the 14-day treatment course was superior to the 7-day treatment. Because of the higher antibiotic resistance rates, in developing countries such as Iran, the 14-day treatment regimens is preferred. It has been shown that the large doses of antibiotics used in the triple therapy change the normal bowel flora. This may result in further gastrointestinal adverse events (8, 9). Clidinium bromide in combination with chlordiazepoxide (clidinium –C) is an anticholinergic drug which may help symptoms of cramping and abdominal stomach pain by decreasing gastric acid secretion and slowing the intestinal movement (10). Chlordiazepoxide component of this drug exerts anxiolytic, sedative, hypnotic, anticonvulsant and skeletal muscle relaxant effects. The drug may inhibit monosynaptic and polysynaptic reflexes by acting as an inhibitory neuronal transmitter or by blocking excitatory synaptic transmission. This drug may also directly depress motor nerve and muscle function. The aim of this study was to assess the effect of clidinium-C on HP eradication with a triple therapy including omeprazole, clarithromycin and amoxicillin (OCA) in patients with peptic ulcer disease (PUD). The secondary aim of the study was to investigate the efficacy and safety of clidinium-C in the prevention of side-effects related to HP eradication.

Background Helicobacter suis is a very fastidious microorganism associated with gastritis, gastric ulcers, and mucosa-associated lymphoid tissue lymphoma in humans. In vitro isolation of this agent from human patients has so far been unsuccessful. Materials and methods A probe-based real-time PCR (RT-PCR) for the rapid detection of H. suis in gastric biopsies was developed. Secondly, a mouse-passage-based protocol was optimized for isolation of low numbers of viable H. suis bacteria. Mice were inoculated with different numbers of viable H. suis (102 -108 ) and kept for 4 weeks to allow multiplication of this pathogen. Results The probe-based real-time PCR (RT-PCR) exhibited a high degree of diagnostic specificity and analytical sensitivity, high linear correlations (r2 between 0.995 and 0.999), and high amplification efficiencies (>90%) for H. suis. No cross-reactivity was detected with human, porcine, non-human primate, and murine DNA nor with DNA from other bacteria including Helicobacter spp. and Campylobacter spp. H. suis was successfully re-isolated from the stomach of mice inoculated with at least 104 viable H. suis, using a biphasic medium (pH 5), consisting of Brucella agar with Brucella broth on top, both supplemented with vitox supplement, Campylobacter-selective supplement, amphotericin (5 μg/mL), HCl (0.05%), fetal bovine serum (20%), and linezolid (5 μg/mL). Linezolid was necessary to inhibit proliferation of contaminants, including lactobacilli. Conclusion The methods described above can be implemented for detection or isolation of H. suis from human gastric biopsies.

Urea breath test (UBT), as a leading preferred non-invasive diagnostic technology, but may not be able to detect oral H. pylori. With negative results of UBT, the patient may have an oral infection. On the basis of the fact of success, eradication rate may increase by 21% in the 95% Cl range after the elimination of oral H. pylori, the author believes oral H. pylori does exist and the oral cavity is the second colonized site aside its primary site of the stomach. H. pylori migrated out of Africa along with its human host circa 60 000 years ago; they are not lives in stomach only. In this review article, evidence established in recent years studies with use more appropriate technology had been listed and discussed. The author considers the oral cavity is a black hole for H. pylori infection that significant effective on gastroenterology and another medical field. The role of the oral cavity as the source of H. pylori infection is so controvert in past years. It seems like a human being having a second-time face to discover H. pylori in the history. H. pylori infection in the mouth could prevent eradication of the infection in the stomach and explain its high recurrence rate. In most cases, infection with the bacterium H. pylori is harmless, but many infected individuals develop stomach ulcers or gastric cancer. In a recent review John Yee of the Research Lab of Oral H. pylori, Everett, USA, argues that oral H. pylori needs to be tackled to clear the bacteria in the stomach. A new H. pylori saliva test is aiding the detection of oral infection and several studies have found a strong association between oral and stomach infection. Yee proposes concomitantly treating the oral infection through professional plaque removal and oral hygiene procedures, and treating the gastric infection with antibiotics. Increasing awareness of oral H. pylori infection could help prevent oral transmission.

Gastric infection by Helicobacter pylori is the most common cause of ulcer disease and gastric cancer. The mechanism of progression from gastritis and inflammation to ulcers and cancer in a fraction of those infected is not definitively known. Significant acidity is unique to the gastric environment and is required for ulcer development. The interplay between gastric acidity and H. pylori pathogenesis is important in progression to advanced disease. The aim of this study was to characterize the impact of acid on gastric epithelial integrity and cytokine release and how H. pylori infection alters these responses. Human gastric epithelial (HGE-20) cells were grown on porous inserts, and survival, barrier function, and cytokine release were studied at various apical pH levels in the presence and absence of H. pylori. With apical acidity, gastric epithelial cells demonstrate increased barrier function, as evidenced by increased transepithelial electrical resistance (TEER) and decreased paracellular permeability. This effect is reduced in the presence of wild-type, but not urease knockout, H. pylori. The epithelial inflammatory response is also modulated by acidity and H. pylori infection. Without H. pylori, epithelial IL-8 release decreases in acid, while IL-6 release increases. In the presence of H. pylori, acidic pH diminishes the magnitude of the previously reported increase in IL-8 and IL-6 release. H. pylori interferes with the gastric epithelial response to acid, contributing to altered barrier function and inflammatory response. H. pylori diminishes acid-induced tightening of cell junctions in a urease-dependent manner, suggesting that local pH elevation promotes barrier compromise and progression to mucosal damage.

Helicobacter pylori (H. pylori) has been found in dental plaque, saliva and lingual sites. To date, taste or olfaction disorders related to H. pylori infections have never been reported. In a review of the literature we found two papers just referring to a sour taste sensation during H. pylori infection. Studies in animal models suggest that changes in taste perception may relate to infections which damage taste buds. We observed an interesting clinical case of a 24-year-old Ghanaian woman with documented H. pylori gastric infection, complaining of cacosmia and cacogeusia. Taste evaluation indicated hypogeusia and highlighted a specific difficulty in discriminating between bitter and acid tastes. Saliva fluid was found positive for the ureA gene (H. pylori ureasi A). On the basis of this report, we hypothesize that taste perception might be correlated with a documented H. pylori infection. So, in a dyspeptic clinical picture in both pre and post diagnostic phase when H. pylori infection is suspected, taste evaluation might be important. Further studies are certainly needed in a large patient population to clarify the possible connection between H. pylori infection and smell-taste distortion.

Since the first description of the human pathogen Helicobacter pylori in the early 1980s, the number of known species in the genus Helicobacter has increased largely. Currently, 45 different Helicobacter species have been identified. Bacteria belonging to this genus can roughly be divided into two major groups, gastric and enterohepatic species. Gastric helicobacters express urease at a high level which helps them to survive in the acidic environment of the stomach, whereas most enterohepatic helicobacters do not. The best-known gastric Helicobacter species is H. pylori. This chapter, however, deals with non-H. pylori helicobacters (NHPH). Most NHPH are animal-associated bacteria, but some of them are of zoonotic significance. First, gastric infections with these bacteria in humans are considered. Thereafter, an overview of natural and experimental gastric infections in animal hosts is given, with emphasis on the gastric helicobacters that are mainly associated with dogs, cats, and pigs. Finally, enterohepatic Helicobacter species are briefly discussed.

Antibiotics have a short residence time and have low concentrations when absorbed through the basolateral membrane in the stomach; this causes a failure to enhance drug concentrations at Helicobacter pylori infection sites. This study developed a nanocarrier system with the ability to carry amoxicillin to increase its efficacy against H. pylori . We used a water-in-oil emulsification system to prepare a positively charged nanoemulsion particle composed of amoxicillin, chitosan, and heparin. The particle size of the prepared nanoemulsion particle was controlled by the constituted compositions. The morphology of the nanoemulsion particles was spherical. In vitro analysis of amoxicillin released indicated that the nanocarrier system controlled amoxicillin release in the gastrointestinal dissolution medium and amoxicillin-loaded nanoemulsion particles localized to the site of H. pylori infection. Meanwhile, results of in vivo clearance assays indicated that the prepared amoxicillin-loaded nanoemulsion particles had a significantly greater H. pylori clearance effect in the gastric infection mouse model than the amoxicillin solution alone.

The operations which are done by general surgeons, and the way in which they are done, have undergone radical change during the last 2 decades, yet the impacts on residency training have not been generally recognized. The change has come about because of 2 principal factors—evolutionary and technological changes, which have occurred in the treatment of several common diseases, and the conversion of a major proportion of abdominal surgery from an open to a laparoscopic approach. In addition to the change in the nature of the surgery done, the impact of the 80-hour workweek on resident experiences with urgent and emergent conditions has also been significant. The impact of this on the development of resident independence and autonomy has not been analyzed. This article will attempt to describe qualitatively the nature of the changes, the negative impacts on resident training, and some proposed measures to mitigate the impact. ENVIRONMENTAL AND TECHNOLOGICAL CHANGE IN DISEASE MANAGEMENT Four common disease categories, which involve intraabdominal pathology, have undergone major technological change in management during the last 20 years. Benign Peptic Ulcer Disease Benign gastric and duodenal ulcer disease has been a staple of general surgical management for decades, for treatment of the complications of bleeding, perforation, and intractability. Three advances in medical treatment have markedly altered the incidence of these complications, and the consequent need for surgical intervention: H2 receptor blockers, proton pump inhibitors, and treatment of Helicobacter pylori gastric infection. As a result of medical management with these 3 modalities, intractability of ulcer disease has virtually disappeared, and perforation and hemorrhage have been markedly reduced. The result is that surgery is infrequently necessary today for treatment of peptic ulcer complications and resident experience with gastric surgery is largely limited to malignancy and other less common conditions. Interestingly, the increase in laparoscopic bariatric surgery has provided the bulk of a typical resident experience in gastric surgery in recent years, but exposure to these procedures is highly variable, and residents are rarely the operating surgeon in these complex technical procedures.

Helicobacter spp. have been detected in different parts of gastrointestinal tract of dogs including the oral cavity, stomach, intestines and recently, hepatobilliary system. However, the transmission pathways of Helicobacter spp. have not been yet fully elucidated. Research in the last decade has proposed that oral–oral and fecal–oral transmissions, among others, may be a plausible route of this gastric infection. This study was carried out primarily to determine the existence of pylori and non-pylori Helicobacter spp. in the oral secretions and dental plaque of stray dogs of Iran as one of the possible routes of humans and animal infection and, secondly, to evaluate the accordance between oral and gastric colonization of Helicobacter spp. in these dogs. Forty-eight adult stray dogs were studied by PCR using 16S rRNA, Helicobacter felis, Helicobacter heilmannii, and Helicobacter pylori specific primers. Positive samples for 16S rRNA specific primers that did not meet the specified species of Helicobacter genus were randomly subjected to sequencing. Helicobacter spp. DNA was found in the oral and gastric specimens of 100 % of the stray dogs. There was not, however, any agreement between Helicobacter colonization at these two locations, at neither genus nor species level. Our study confirmed that the oral cavity of stray dogs routinely exposed to transient forms of bacteria and may temporarily harbor Helicobacter spp and Wolinella spp. Therefore, oral cavity as a source of Helicobacter spp. may act as a reservoir for transmission. However, it may not necessarily reflect the colonization status of the gastric mucosa.