Helicobacter Pylori Secreted Peptidyl Prolyl Cis, Trans-isomerase Drives Th17 Inflammation in Gastric Adenocarcinoma

Overview

Journal Intern Emerg Med

Publisher Springer

Specialties Emergency Medicine
General Medicine

Date 2012 Oct 12

PMID 23054412

Citations 70

Authors

Amedeo Amedei

Fabio Munari

Chiara Della Bella

Elena Niccolai

Marisa Benagiano

Lapo Bencini

Fabio Cianchi

Marco Farsi

Giacomo Emmi

Giuseppe Zanotti

Marina de Bernard

Manikuntala Kundu

Mario Milco DElios

Affiliations

Soon will be listed here.

Abstract

Helicobacter pylori infection is characterized by an inflammatory infiltrate, consisting mainly of neutrophils and T cells. This study was undertaken to evaluate the type of gastric T cell response elicited by the secreted peptidyl prolyl cis, trans-isomerase of H. pylori (HP0175) in patients with distal gastric adenocarcinoma. The cytokine profile and the effector functions of gastric tumor-infiltrating lymphocytes (TILs) specific for HP0175 was investigated in 20 patients with distal gastric adenocarcinoma and H. pylori infection. The helper function of HP0175-specific TILs for monocyte MMP-2, MMP-9, and VEGF production was also investigated. TILs cells from H. pylori infected patients with distal gastric adenocarcinoma produced Interleukin (IL)-17 and IL-21 in response to HP0175. HP0175-specific TILs showed poor cytolytic activity while expressing helper activity for monocyte MMP-2, MMP-9 and VEGF production. These findings indicate that HP0175 is able to drive gastric Th17 response. Thus, HP0175, by promoting pro-inflammatory low cytotoxic TIL response, matrix degradation and pro-angiogenic pathways, may provide a link between H. pylori and gastric cancer.

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