title: Interleukin-22 promotes T helper 1 (Th1)/Th17 immunity in chlamydial lung infection.
abstract: The role of interleukin-22 (IL-22) in intracellular bacterial infections is a controversial issue, although the contribution of this cytokine to host defense against extracellular bacterial pathogens has been well established. In this study, we focused on an intra-cellular bacterium, Chlamydia, and evaluated the production and function of IL-22 in host defense against chlamydial lung infection using a mouse model. We found that Chlamydia muridarum infection elicited quick IL-22 responses in the lung, which increased during infection and were reduced when bacterial loads decreased. More importantly, blockade of endogenous IL-22 using neutralizing anti-IL-22 monoclonal antibodies (mAb) resulted in more severe disease in the mice, leading to significantly higher weight loss and bacterial growth and much more severe pathological changes than treatment with isotype control antibody. Immunological analyses identified significantly lower T helper 1 (Th1) and Th17 responses in the IL-22-neutralized mice. In contrast, intranasal administration of exogenous IL-22 significantly enhanced protection following chlamydial lung infection, which was associated with a significant increase of Th17 response. The data demonstrate that IL-22 is a critical cytokine, mediating host defense against chlamydial lung infection and coordinating the function of distinct Th-cell subsets, particularly Th1 and Th17, in the process.
authors: Departments of Medical Microbiology and Immunology, University of Manitoba, Winnipeg, Manitoba, Canada Department of Medical Microbiology, Shandong University School of Medicine, Jinan, Shandong, PR China.
authors: Ying
authors: Y
authors: Peng
authors: Departments of Medical Microbiology and Immunology, University of Manitoba, Winnipeg, Manitoba, Canada.
authors: Xiaoling
authors: X
authors: Gao
authors: Departments of Medical Microbiology and Immunology, University of Manitoba, Winnipeg, Manitoba, Canada.
authors: Jie
authors: J
authors: Yang
authors: Departments of Medical Microbiology and Immunology, University of Manitoba, Winnipeg, Manitoba, Canada.
authors: Sudhanshu
authors: S
authors: Shekhar
authors: Departments of Medical Microbiology and Immunology, University of Manitoba, Winnipeg, Manitoba, Canada.
authors: Shuhe
authors: S
authors: Wang
authors: Departments of Medical Microbiology and Immunology, University of Manitoba, Winnipeg, Manitoba, Canada.
authors: Yijun
authors: Y
authors: Fan
authors: Department of Medical Microbiology, Shandong University School of Medicine, Jinan, Shandong, PR China.
authors: Weiming
authors: W
authors: Zhao
authors: Departments of Medical Microbiology and Immunology, University of Manitoba, Winnipeg, Manitoba, Canada.
authors: Xi
authors: X
authors: Yang
mesh_terms: D000818:Animals; D002690:Chlamydia Infections / Q000235:genetics / Q000276:immunology* / Q000473:pathology; D023502:Chlamydia muridarum; D016207:Cytokines / Q000235:genetics / Q000276:immunology*; D008168:Lung / Q000276:immunology / Q000473:pathology; D008171:Lung Diseases / Q000235:genetics / Q000276:immunology* / Q000473:pathology; D008198:Lymph Nodes / Q000276:immunology; D008297:Male; D008810:Mice, Inbred C57BL; D012333:RNA, Messenger; D013154:Spleen / Q000276:immunology; D018417:Th1 Cells / Q000276:immunology*; D058504:Th17 Cells / Q000276:immunology*
chemical_list: D016207:Cytokines; D012333:RNA, Messenger