3 years ago

Interleukin-17C in human Helicobacter pylori gastritis.

Graham DY, Yamaoka Y, Vilaichone RK, Uchida T, Mahachai V, Uotani T, Nagashima H, Jiménez Abreu JA, Tanaka S, Tshering L, Ratanachu-Ek T, Cruz M
The interleukin-17 (IL-17) family of cytokines (IL-17A-F) is involved in many inflammatory diseases. Although IL-17A is recognized as being involved in the pathophysiology of H. pylori-associated diseases, the role of other IL-17 cytokine family members remains unclear. Microarray analysis of IL-17 family cytokines was performed in H. pylori-infected and uninfected gastric biopsy specimens. IL-17C mRNA was upregulated approximately 4.5-fold in H. pylori-infected gastric biopsies. This was confirmed by quantitative reverse transcriptase-polymerase chain reaction in infected and uninfected gastric mucosa obtained from Bhutan and from the Dominican Republic. Immunohistochemical analysis showed that IL-17C expression in H. pylori-infected gastric biopsies was predominantly localized to epithelial and chromogranin A-positive endocrine cells. IL-17C mRNA levels were also significantly greater among cagA-positive than cagA-negative H. pylori infections (P = 0.012). In vitro studies confirmed an increase in IL-17C mRNA and protein levels in cells infected with cagA-positive infections compared to cells infected either cagA-negative or cag PAI mutants. Chemical inhibition of IKK, MEK and JNK inhibited induction of IL-17C proteins in infected cells whereas p38 inhibition had no effect on IL-17C protein secretion. In conclusion, H. pylori infection was associated with a significant increase in IL-17C expression in human gastric mucosa. The role of IL-17C in the pathogenesis of H. pylori-induced diseases remains to be determined.

Publisher URL: https://www.ncbi.nlm.nih.gov/pubmed/28739826

DOI: PubMed:28739826

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