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Innate immunity components and cytokines in gastric mucosa in children with Helicobacter pylori infection. | LitMetric

Innate immunity components and cytokines in gastric mucosa in children with Helicobacter pylori infection.

Mediators Inflamm

Department of Clinical Microbiology and Immunology, The Children's Memorial Health Institute, Aleja Dzieci Polskich 20, 04-730 Warsaw, Poland ; Institute of Nursery and Public Health, Rzeszow University, Al. Rejtana 16A, 35-310 Rzeszow, Poland.

Published: February 2016

AI Article Synopsis

  • The study aimed to examine how components of innate immunity and cytokines are expressed in the gastric mucosa of children infected and uninfected with H. pylori.
  • It found that while specific immunity receptors showed no significant increase, H. pylori infection was linked to higher levels of certain cytokines like IL-6, IL-10, IFN-γ, and TNF-α, with variations based on the strain type (cagA+ vs. cagA-).
  • The results suggest that H. pylori infection tends to produce a Th1 immune response, limited upregulation of natural immunity receptors, and a predominate anti-inflammatory response, potentially explaining the mild gastric inflammation common in infected kids.

Article Abstract

PURPOSE. To investigate the expression of innate immunity components and cytokines in the gastric mucosa among H. pylori infected and uninfected children. Materials and Methods. Biopsies of the antral gastric mucosa from children with dyspeptic symptoms were evaluated. Gene expressions of innate immunity receptors and cytokines were measured by quantitative real-time PCR. The protein expression of selected molecules was tested by immunohistochemistry. RESULTS. H. pylori infection did not lead to a significant upregulation of MyD88, TLR2, TLR4, CD14, TREM1, and TREM2 mRNA expression but instead resulted in high mRNA expression of IL-6, IL-10, IFN-γ, TNF-α, and CD163. H. pylori cagA(+) infection was associated with higher IL-6 and IL-10 mRNA expression, as compared to cagA(-) strains. H. pylori infected children showed increased IFN-γ and TNF-α protein levels. IFN-γ mRNA expression correlated with both H. pylori density of colonization and lymphocytic infiltration in the gastric mucosa, whereas TNF-α protein expression correlated with bacterial density. CONCLUSION. H. pylori infection in children was characterized by (a) Th1 expression profile, (b) lack of mRNA overexpression of natural immunity receptors, and (c) strong anti-inflammatory activities in the gastric mucosa, possibly resulting from increased activity of anti-inflammatory M2 macrophages. This may explain the mildly inflammatory gastric inflammation often observed among H. pylori infected children.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4407632PMC
http://dx.doi.org/10.1155/2015/176726DOI Listing

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