IL-9 contributes to the host immune response against Helicobacter pylori and helps limit infection in a Mouse Model

As an important mediator in lots of diseases, interleukin-9 (IL-9) can be a protector or pro-inflammatory cytokine depending on the complicated inflammatory milieu. Helicobacter pylori (H. pylori) induced a series of immunology cells and cytokines change, and however, the role of IL-9 in H. pylori infection remains unknown.

Wild-type and IL-9 deficient mice were infected with H. pylori by means of intragastric administration. The colonization of H. pylori bacteria was measured by detecting specific 16s rDNA, and the intensity of inflammation was observed by H&E stain. The expression level of inflammation cytokines was determined by ELISA and quantitative real-time PCR.

IL-9 was increased due to the attack of H. pylori, besides deletion of Il9 aggravated the bacterial colonization and inflammation intensity. In addition, treatment of rmIL-9 reduced colonized H. pylori and inflammation level, indicated that IL-9 was a protector for the host against this bacterium. Followed by the H. pylori infection, interferon (IFN)-γ and interleukin (IL)-17A were up-regulated as expected, and nevertheless, the expression of IL-17A shared a positive relationship with IL-9 while IFN-γ negative associated with IL-9. Moreover, we also proved that Treg cells were not involved in the protective effect of IL-9, and meanwhile, CD4⁺ CD25^- T cells secreted more IFN-γ and less IL-17A in vitro due to the deletion of Il9.

IL-9 plays a protective role against H. pylori and the protection associated with cytokines change including IFN-γ and IL-17A.