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Link to original content: http://pubmed.ncbi.nlm.nih.gov/38231216/
Immune Biology and Persistence of Helicobacter pylori in Gastric Diseases - PubMed Skip to main page content
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. 2023:444:83-115.
doi: 10.1007/978-3-031-47331-9_4.

Immune Biology and Persistence of Helicobacter pylori in Gastric Diseases

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Immune Biology and Persistence of Helicobacter pylori in Gastric Diseases

Sonja Fuchs et al. Curr Top Microbiol Immunol. 2023.

Abstract

Helicobacter pylori is a prevalent pathogen, which affects more than 40% of the global population. It colonizes the human stomach and persists in its host for several decades or even a lifetime, if left untreated. The persistent infection has been linked to various gastric diseases, including gastritis, peptic ulcers, and an increased risk for gastric cancer. H. pylori infection triggers a strong immune response directed against the bacterium associated with the infiltration of innate phagocytotic immune cells and the induction of a Th1/Th17 response. Even though certain immune cells seem to be capable of controlling the infection, the host is unable to eliminate the bacteria as H. pylori has developed remarkable immune evasion strategies. The bacterium avoids its killing through innate recognition mechanisms and manipulates gastric epithelial cells and immune cells to support its persistence. This chapter focuses on the innate and adaptive immune response induced by H. pylori infection, and immune evasion strategies employed by the bacterium to enable persistent infection.

Keywords: H. pylori; Immune evasion; Immune response; Persistence.

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References

    1. Akhiani AA, Schon K, Franzen LE, Pappo J, Lycke N (2004a) Helicobacter pylori-specific antibodies impair the development of gastritis, facilitate bacterial colonization, and counteract resistance against infection. J Immunol 172:5024–5033. https://doi.org/10.4049/jimmunol.172.8.5024 - DOI - PubMed
    1. Akhiani AA, Schon K, Lycke N (2004b) Vaccine-induced immunity against Helicobacter pylori infection is impaired in IL-18-deficient mice. J Immunol 173:3348–3356. https://doi.org/10.4049/jimmunol.173.5.3348 - DOI - PubMed
    1. Akhiani AA, Stensson A, Schon K, Lycke NY (2005) IgA antibodies impair resistance against Helicobacter pylori infection: studies on immune evasion in IL-10-deficient mice. J Immunol 174:8144–8153. https://doi.org/10.4049/jimmunol.174.12.8144 - DOI - PubMed
    1. Al-Sammak F, Kalinski T, Weinert S, Link A, Wex T, Malfertheiner P (2013) Gastric epithelial expression of IL-12 cytokine family in Helicobacter pylori infection in human: is it head or tail of the coin? PLoS ONE 8:e75192. https://doi.org/10.1371/journal.pone.0075192 - DOI - PubMed - PMC
    1. Algood HM, Gallo-Romero J, Wilson KT, Peek RM Jr, Cover TL (2007) Host response to Helicobacter pylori infection before initiation of the adaptive immune response. FEMS Immunol Med Microbiol 51:577–586. https://doi.org/10.1111/j.1574-695X.2007.00338.x - DOI - PubMed

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