3 years ago

Interleukin 17A Aggravates Middle Ear Injury Induced by Streptococcus Pneumoniae through p38 MAPK Signaling Pathway.

He Y, Zhang X, Xiang Y, Yin Y, Fan F, Wang Z, Liu W, Wang W, Huang Y, Ma Y, Liu J, Jin C, Xu W
Acute otitis media (AOM) is one of the most common bacterial infection diseases in children aged 2-7 yr worldwide. We previously demonstrated that interleukin (IL)-17A promotes an acute inflammatory response characterized by the influx of neutrophils into the middle ear cavity during Streptococcus pneumoniae (Spn)-induced AOM. Generally, inflammatory response is viewed as an effector that frequently causes local tissue damage. However, little is known about the pathogenic effects of IL-17A in AOM. Here, we investigated the pathogenic effects of IL-17A by using wild-type (WT) and IL-17A knockout (KO) mouse models. Results showed that pathogenic effects of AOM, including weight loss, histopathological changes and pro-inflammatory cytokine production, were more severe in WT mice than in IL-17A KO mice, suggesting that IL-17A aggravates tissue damage in AOM. Furthermore, these pathogenic effects were found to be dependent on p38 mitogen-activated protein kinase (MAPK) and could be reversed in the presence of p38 MAPK specific inhibitor. It is also demonstrated that IL-17A promoted the production of neutrophil myeloperoxidase (MPO) through p38 MAPK signaling pathway, which was responsible for the middle ear tissue injury. These data support the conclusion that IL-17A contributes to the middle ear injury through the p38 MAPK signaling pathway.

Publisher URL: https://www.ncbi.nlm.nih.gov/pubmed/28739823

DOI: PubMed:28739823

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