Abstract
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.
Highlights
IL-9 is a cytokine which has been identified and characterized for more than two decades[1]
C. muridarum was grown in HeLa 229 cells in RPMI 1640 medium supplemented with 10% fetal bovine serum (FBS), 1% L-glutamine and 25mg/ml gentamycin, and the elementary bodies (EBs) were purified by discontinuous density gradient centrifugation
The results suggest that IL-9 can potentially influence IL-17 and IFN-γ responses in Chlamydia muridarum (Cm) infection
Summary
IL-9 is a cytokine which has been identified and characterized for more than two decades[1]. IL-9 is involved in parasitic infections, allergy, and inflammatory processes[1]. Initially considered as a Th2 cytokine, IL-9 can be produced by many other cells especially T cell subsets including Th1, Th17, Th22 and regulatory T (Treg). A specific CD4 T cell linage, Th9, is found to predominantly produce IL-9[2]. PU. and interferon regulatory factor 4 (IRF4) are the typical transcription factor for Th9 development. Differentiation of Th9 is dependent on the presence of IL-4 and transforming growth factor-β (TGF-β) in the microenvironment[3]. In addition to CD4 T cells, it is recently reported that innate lymphoid cells (ILC) could be a major source
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