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Although IL-17A is recognized as being involved in the pathophysiology of<jats:named-content content-type=\"genus-species\">Helicobacter pylori<\/jats:named-content>-associated diseases, the role of other IL-17 cytokine family members remains unclear. Microarray analysis of IL-17 family cytokines was performed in<jats:named-content content-type=\"genus-species\">H. pylori<\/jats:named-content>-infected and uninfected gastric biopsy specimens.<jats:italic>IL-17C<\/jats:italic>mRNA was upregulated approximately 4.5-fold in<jats:named-content content-type=\"genus-species\">H. pylori<\/jats:named-content>-infected gastric biopsy specimens. This was confirmed by quantitative reverse transcriptase PCR in infected and uninfected gastric mucosa obtained from Bhutan and from the Dominican Republic. Immunohistochemical analysis showed that IL-17C expression in<jats:named-content content-type=\"genus-species\">H. pylori<\/jats:named-content>-infected gastric biopsy specimens was predominantly localized to epithelial and chromogranin A-positive endocrine cells.<jats:italic>IL-17C<\/jats:italic>mRNA levels were also significantly greater among<jats:italic>cagA<\/jats:italic>-positive than<jats:italic>cagA<\/jats:italic>-negative<jats:named-content content-type=\"genus-species\">H. pylori<\/jats:named-content>infections (<jats:italic>P<\/jats:italic>= 0.012).<jats:italic>In vitro<\/jats:italic>studies confirmed an increase in<jats:italic>IL-17C<\/jats:italic>mRNA and protein levels in cells infected with<jats:italic>cagA<\/jats:italic>-positive infections compared to cells infected with either<jats:italic>cagA<\/jats:italic>-negative or<jats:italic>cag<\/jats:italic>pathogenicity island (PAI) mutant. Chemical inhibition of I\u03baB kinase (IKK), mitogen-activated protein extracellular signal-regulated kinase (MEK), and Jun N-terminal kinase (JNK) inhibited induction of IL-17C proteins in infected cells, whereas p38 inhibition had no effect on IL-17C protein secretion. In conclusion,<jats:named-content content-type=\"genus-species\">H. pylori<\/jats:named-content>infection was associated with a significant increase in IL-17C expression in human gastric mucosa. The role of IL-17C in the pathogenesis of<jats:named-content content-type=\"genus-species\">H. pylori<\/jats:named-content>-induced diseases remains to be determined.<\/jats:p>","DOI":"10.1128\/iai.00389-17","type":"journal-article","created":{"date-parts":[[2017,7,25]],"date-time":"2017-07-25T00:20:22Z","timestamp":1500942022000},"update-policy":"https:\/\/doi.org\/10.1128\/asmj-crossmark-policy-page","source":"Crossref","is-referenced-by-count":25,"title":["Interleukin-17C in Human Helicobacter pylori Gastritis"],"prefix":"10.1128","volume":"85","author":[{"given":"Shingo","family":"Tanaka","sequence":"first","affiliation":[{"name":"Department of Medicine, Michael E. DeBakey Veterans Affairs Medical Center and Baylor College of Medicine, Houston, Texas, USA"},{"name":"Department of Environmental and Preventive Medicine, Oita University Faculty of Medicine, Yufu, Japan"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Hiroyuki","family":"Nagashima","sequence":"additional","affiliation":[{"name":"Department of Medicine, Michael E. 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