Acinetobacter baumannii reinforces the pathogenesis by promoting IL-17 production in a mouse pneumonia model

AbstractInterleukin-17 (IL-17) is involved in host defense against bacterial infection.  Little is known about the role of IL-17 inA. baumannii-infected pneumonia. Our objective was to investigate the role of IL-17 in pulmonaryA. baumannii infection in a mouse model. We infected C57BL/6 mice intra-tracheally (i.t.) withA. baumannii to establish pneumonia model and foundA. baumannii infection elevated IL-17 expression in lungs. IL-17-deficient (Il17−/−) mice were resistant to pulmonaryA. baumannii infection, showing improved mice survival, reduced bacteria burdens, and alleviated lung inflammation.  Further, treatment ofA. baumannii-infectedIl17−/− mice with IL-17 exacerbated the severity of pneumonia. These data suggest a pathogenic role of IL-17 in pulmonaryA. baumannii infection. Further, the infiltration and phagocytic function of neutrophils in broncho-alveolar lavage fluid were detected by flow cytometry. The results showed thatIl17−/− mice had increased neutrophil infiltration and enhanced phagocytosis in neutrophils at the early time of infection. Treatment of mice with IL-17 suppressed phagocytic function of neutrophils. All data suggest that IL-17 promotes susceptibility of mice to pulmonaryA. baumannii infection by suppressing neutrophil phagocytosis at early time of infection. Targeting IL-17 might be a potential therapeutic strategy in controlling the outcome ofA. baumannii pneumonia.
Source: Medical Microbiology and Immunology - Category: Microbiology Source Type: research