Abstract

Objective To investigate the effects of IL-17-producing γδT cells on accumulation and chemotaxis of neutrophils in lung following Chlamydia muridarum (Cm) airway infection and the possible mechanism. Methods Wild type (WT) (C57BL/6) and TCRδ-/- mice were inoculated intranasally with 3×103 inclusion-forming units (IFU) of Cm strains to induce Chlamydial pneumonitis in mice. Mononuclear cells were isolated from the lungs of mice at early stage of chlamydial infection. The percentages of Gr1+ CD11b+ neutrophils in lung mononuclear cells were detected by flow cytometry. The levels of IL-17 secreted by γδT cells were measured with intracellular cytokine staining. The expression of IL-17, KC and IL-6 at mRNA level in lungs were measured by RT-PCR. Results Our data showed that γδT cells in lung tissues were activated rapidly and secreted large quantities of IL-17 at early stage of Cm infection. Compared with uninfected mice, the production of IL-17 by CD3+ γδT+ cells in infected mice significantly increased and reached the peak on the third day (P<0.001), and the levels of IL-17 remained high at 7 days post-infection (p.i.) (P<0.05). Compared with WT(C57BL/6) mice, TCRδ-/- mice showed decreased expression of IL-17 at mRNA level and lower percentages of CD11b+ Gr-1+ neutrophils in lungs at early stage of Cm infection (3 days p. i.). Further analysis showed that the expression of KC and IL-6 at mRNA level significantly decreased at 3 and 7 days after Cm infection. Conclusion IL-17-producing γδT cells might promote infiltration of neutrophils to lung tissues by promoting the expression of KC and IL-6 during Chlamydial pneumonitis. Key words: Chlamydia muridarum; Neutrophils; γδT cells; IL-17

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