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The Relationship between Toll-like Receptors and Helicobacter pylori-Related Gastropathies: Still a Controversial Topic.

ABSTRACT: Innate immunity represents the first barrier against bacterial invasion. Toll-like receptors (TLRs) belong to the large family of pattern recognition receptors (PRRs), and their activation leads to the induction of inflammatory cytokines, chemokines, antigen-presenting molecules, and costimulatory molecules. Recent studies have focused on identifying the association between TLRs and Helicobacter pylori- (H. pylori-) related diseases. Therefore, this minireview focuses on assessing the role of these TLRs in the development of H. pylori-related gastropathies. Both TLR2 and TLR were found to be involved in H. pylori LPS recognition, with contradictory results most likely due to both the inability to obtain pure LPS in experimental studies and the heterogeneity of the bacterial LPS. In addition, TLR2 was found to be the most extensively expressed gene among all the TLRs in gastric tumors. High levels of TLR4 were also associated with a higher risk of gastric cancer. TLR5 was initially associated with the recognition of H. pylori flagellin, but it seems that this bacterium has developed mechanisms to escape this recognition representing an important factor involved in the persistence of this infection and subsequent carcinogenesis. TLR9, the only TLR with both anti- and proinflammatory roles, was involved in the recognition of H. pylori DNA. The dichotomous role of TLR9, promoting or suppressing the infection, depends on the gastric environment. Recently, TLR7 and TLR8 were shown to recognize purified H. pylori RNA, thereby inducing proinflammatory cytokines. TLR1 and TLR10 gene polymorphisms were associated with a higher risk for gastric cancer in H. pylori-infected individuals. Different gene polymorphisms of these TLRs were found to be associated with gastric cancer depending mostly on ethnicity. Further studies are required in order to develop preventive and therapeutic strategies against H. pylori infections based on the functions of TLRs.

SUBMITTER: Melit LE

PROVIDER: S-EPMC6378784 | biostudies-literature | 2019

REPOSITORIES: biostudies-literature

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The Relationship between Toll-like Receptors and Helicobacter pylori-Related Gastropathies: Still a Controversial Topic.

Meliț Lorena Elena LE Mărginean Cristina Oana CO Mărginean Cristian Dan CD Mărginean Maria Oana MO

Journal of immunology research 20190204

Innate immunity represents the first barrier against bacterial invasion. Toll-like receptors (TLRs) belong to the large family of pattern recognition receptors (PRRs), and their activation leads to the induction of inflammatory cytokines, chemokines, antigen-presenting molecules, and costimulatory molecules. Recent studies have focused on identifying the association between TLRs and Helicobacter pylori- (H. pylori-) related diseases. Therefore, this minireview focuses on assessing ...[more]

PMID: 30863783

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Project description:Background: Penicillins inhibit cell wall synthesis; therefore, H. pylori must be dividing for these antibiotics to be effective. Identifying growth responses to varying medium pH may allow design of more effective treatment regimens. Aim: To determine the effect of acidity on bacterial growth and the bactericidal efficacy of ampicillin. Methods: H. pylori were incubated in dialysis chambers suspended in 1.5L of media at various pHs with 5mM urea, with or without ampicillin, for 4, 8 or 16 hours, thus mimicking unbuffered gastric juice. Changes in gene expression, viability and survival were determined. The bacterial load of H. pylori infected gerbils was determined with and without profound acid inhibition. Results: At pH 3.0, but not at pH 4.5 or 7.4, there was decreased expression of ~400 genes, including many cell envelope biosynthesis, cell division genes and penicillin-binding proteins. In the presence of ampicillin, viability and survival declined at pH 4.5 and 7.4 but not at pH 3.0. Profound acid inhibition of H. pylori infected gerbils increased the antral bacterial load >3 fold, showing that elevation of intragastric pH stimulated growth. Conclusions: Ampicillin is bactericidal at pH 4.5 and 7.4, but not at pH 3.0, due to decreased expression of cell envelope and division genes at pH 3.0. Therefore, at pH 3.0, the pH at the gastric surface, the bacteria are non-dividing and persist with ampicillin treatment. A more effective inhibitor of acid secretion that maintains gastric pH near neutrality for 24 hours/day should enhance the efficacy of triple therapy and of amoxicillin, even allowing dual therapy for H. pylori eradication. There were a total of three biological replicates, each containing one control (incubated at pH 7.4) and one acidic (pH 3.0) sample, whose RNA were extracted on different dates. Microarray studies performed on these six samples were done in triplicate. One of the triplicates for two of the biological control triplicates were removed from the data set due to poor hybridization

Project description:OBJECTIVES:Many studies have explored the association between Helicobacter pylori infection and osteoporosis. However, the results remain controversial. Therefore, we performed this systematic review and meta-analysis to evaluate the association between H. pylori infection and osteoporosis. DESIGN:Systematic review and meta-analysis of case-control studies. DATA SOURCES:Databases, including PubMed, Embase, Web of Science and Chinese Biomedical Literature Database, were screened from inception to 30 April 2018. ELIGIBILITY CRITERIA:Case-control studies aimed at assessing the association between H. pylori infection and osteoporosis. DATA EXTRACTION AND ANALYSIS:Study characteristics and study quality sections were reviewed. Studies were selected, and data were extracted by two reviewers. Pooled ORs and 95% CIs were calculated using random effects model if heterogeneity existed; otherwise, fixed effects model was used. Subgroup analyses were performed to explore the source of heterogeneity. Publication bias and sensitivity analyses were also tested. RESULTS:A total of 21 studies with 9655 participants were included in our analyses. Taking together, we found that H. pylori infection was associated with increased odds of osteoporosis (OR (95% CI): 1.39 (1.13 to 1.71)); there was no significant difference between osteoporosis and osteopaenia; the association between osteoporosis and H. pylori infection was relatively higher in men than women but did not reach significant level. However, the decrease of bone mineral density in H. pylori-positive patients was not significant when compared with H. pylori negative controls, which may due to the sample size. CONCLUSIONS:Our meta-analysis suggests an association between osteoporosis and H. pylori infection. The clinicians should pay more attention to the patients infected with H. pylori. Further studies were still needed to exploring the confounding factors among studies and to elucidate the underlying biological mechanisms.

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The Relationship between Toll-like Receptors and Helicobacter pylori-Related Gastropathies: Still a Controversial Topic.

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The Relationship between Toll-like Receptors and <i>Helicobacter pylori</i>-Related Gastropathies: Still a Controversial Topic.

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