Expression of interleukin-16 in gastric mucosa: a possible role in the persistance of helicobacter pylori infection


Helicobacter pylori (H. pylori) infects the human gastric mucosa of >50% of humankind and causes chronic gastritis, peptic ulcers, and gastric adenocarcinoma. H. pylori infected gastric epithelial cells (GECs) produce an array of chemokines that recruit other cells. IL-16 is potentially a key chemokine not yet examined during H. pylori infection. IL-16 selectively recruits CD4+ T cells since it uses CD4 as a receptor; but makes them unresponsive to antigen, which could explain failed vaccine clinical trials. As T cells from the H. pylori-infected gastric mucosa are hyporesponsive, I wanted to investigate the production of IL-16 by GECs, the mechanisms underlying IL-16 production and the role of gastric IL-16 in the persistent of H. pylori-infection. IL-16 expression by GECs was analyzed using FACS and RT-PCR following infection with H. pylori as well as mediators present during infection. I observed that H. pylori increases expression of IL-16 in different gastric epithelial cell lines. Also, histamine, IL-8 and IFN- increased IL-16 expression. These findings uncover relevant information pertaining to the accumulation of CD4+ T cells that is observed in patients’ gastric mucosa with H. pylori and could explain why clinical trials have failed in efforts to develop a vaccine to this important pathogen.



H. pylori, Gastric Epithelial Cells, Interleukin-16.