IL-21/IL-21R Promotes the Pro-Inflammatory Effects of Macrophages during C. muridarum Respiratory Infection

Interleukin-21 and its receptors (IL-21/IL-21R) aggravate chlamydial lung infection, while macrophages (Mφ) are one of the main cells infected by chlamydia source inflammatory cytokines. Therefore, it is particularly important to study whether IL-21/IL-21R aggravates respiratory infection regulating Mφ. Combined with bioinformatics analysis, we established an IL-21R-deficient (IL-21R−/−) mouse model Chlamydia muridarum (C. muridarum) tract in vivo, studied C. muridarum-stimulated RAW264.7 addition rmIL-21 vitro, conducted adoptive transfer experiments clarify association between IL-21R−/− mice showed lower infiltration pulmonary total Mφ, alveolar macrophages, interstitial compared WT following infection. Transcriptomic analysis suggested that M1-related genes downregulated IL-21R deficiency affects Mφ-mediated response during In vivo verified mice, M1-type CD80+, CD86+, MHC II+, TNFα+, iNOS+ Mφ decreased, there were no differences M2-type CD206+, TGF-β+, IL-10+ ARG1+ administration promoted levels iNOS-NO expression IL-12p40 TNFα, but had effect on TGFβ or IL-10. Further, M1-like bone marrow-derived derived from unlike those effectively protected recipients against induced relieved pathology. These findings help understanding mechanism which exacerbates promoting proinflammatory