Th‐17 response and antimicrobial peptide expression are uniformly expressed in gastric mucosa of Helicobacter pylori‐infected patients independently of their clinical outcomes.

Abstract: Background: The pathological determinism of H. pylori infection is explained by complex interplay between bacterial virulence and host inflammatory response. In a large prospective multicenter clinical study, Th17 response, expression of antimicrobial peptides (AMPs), cagA and vacA status, and bacterial density were investigated in the gastric mucosa of H. pylori ‐infected patients. Materials and methods: Gastric inflammatory response was analyzed by RT‐qPCR for quantification of Th17 cytokines (IL‐17A, IL‐22), CXCL‐8, and AMPs (BD2 and S100A9) mRNA levels in gastric biopsies. Detection and genotyping of H. pylori strains were achieved by bacterial culture and PCR. Results: Among 787 patients screened for H. pylori, 269 were analyzed (147 H. pylori ‐infected and 122 uninfected patients). In H. pylori ‐infected patients, distribution was 83 gastritis, 12 duodenal ulcers, 5 gastric ulcers, and 47 precancerous and cancerous lesions. CXCL‐8, IL‐17A, BD2, and S100A9 mRNA levels were significantly increased in H. pylori ‐infected patients but, surprisingly, IL‐22 was not, and no difference was shown between H. pylori ‐related diseases. A positive correlation was identified between S100A9 expression and bacterial density. Although expression of the virulence genes cagA and vacA did not impact inflammatory response, patients infected with a cagA‐positive strain were associated with severe H. pylori ‐related diseases. Conclusion: This study showed that CXCL‐8, IL‐17A, and AMPs are not differently expressed according to the various H. pylori ‐related diseases. The clinical outcome determinism of H. pylori infection is most likely not driven by gastric inflammation but rather tends to mainly influenced by bacterial virulence factors. [ABSTRACT FROM AUTHOR]