Chlamydial lung infection induces transient IL-9 production which is redundant for host defense against primary infection

• Published in: PloS one Vol. 10; no. 2; p. e0115195
• Main Authors: Peng, Ying, Gao, Xiaoling, Yang, Jie, Shekhar, Sudhanshu, Wang, Shuhe, Fan, Yijun, Yang, Xi
• Format: Journal Article
• Language: English
• Published: United States Public Library of Science 03.02.2015; Public Library of Science (PLoS)
• Subjects: Adaptive immunity; Animals; B cells; Bacteria; Bacterial infections; Biological response modifiers; Body weight; CD4 antigen; Chlamydia; Chlamydia Infections - immunology; Chlamydia Infections - metabolism; Chlamydia muridarum; Chlamydia pneumoniae; Chlamydia trachomatis; Cytokines; Dendritic cells; Health aspects; Helper cells; Immunity; Immunoglobulin A; Immunoglobulin G; Immunology; Infection; Infections; Interferon; Interleukin 17; Interleukin 9; Interleukin-9 - biosynthesis; Intracellular Space - microbiology; Leprosy; Leukocytes (mononuclear); Lung - immunology; Lung - microbiology; Lung - pathology; Lung diseases; Lung Diseases - immunology; Lung Diseases - metabolism; Lungs; Lymphocytes; Lymphocytes T; Male; Medical research; Mice; Mice, Inbred C57BL; Neutralization; Parasitic diseases; Phosphorylation; Pneumonia; Sexually transmitted diseases; Spleen; T cell receptors; T cells; Transcription factors; γ-Interferon; Canada; Manitoba Canada
• ISSN: 1932-6203; 1932-6203
• DOI: 10.1371/journal.pone.0115195

IL-9/Th9 responses are recently found to be important for innate and adaptive immunity particularly in parasitic infections. To date, the study on the role of IL-9 in bacterial infections is limited and the reported data are contradictory. One reported function of IL-9/Th9 is to modulate Th1/Th17 responses. Since our and others' previous work has shown a critical role of Th1 and Th17 cells in host defense against chlamydial lung infection, we here examined the role of IL-9 responses in Chlamydia muridarum (Cm) lung infection, particularly its effect on Th1 and Th17 responses and outcome infection. Our data showed quick but transient IL-9 production in the lung following infection, peaking at day 3 and back to baseline around day 7. CD4+ T cell was the major source of IL-9 production in the lung infection. Blockade of endogenous IL-9 using neutralizing antibody failed to change Interferon-γ (IFN-γ) and IL-17 production by cultured spleen mononuclear cells isolated from Cm infected mice. Similarly, in vivo neutralization of IL-9 failed to show significant effect on T cell (Th1 and Th17) and antibody responses (IgA, IgG1 and IgG2a). Consistently, the neutralization of IL-9 had no significant effect on disease process, including body weight change, bacterial burden and histopathological score. The data suggest that IL-9 production following chlamydial lung infection is redundant for host defense against the intracellular bacteria.