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

Background 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. Materials and methods 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. Results 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 . Conclusions IL‐9 plays a protective role against H .  pylori and the protection associated with cytokines change including IFN‐γ and IL‐17A.