Objective: To evaluate the early interleukin-17 (IL-17) production in airway upon Chlamydia trachomatis infection and its relationship with the secretion of interleukin-6 (IL-6) and macrophage inflammatory protein 2 (MIP-2) in local site.
Methods: In vivo, a murine model of pneumonia induced by intranasal inoculation with Chlamydia trachomatis mouse pneumonitis (MoPn, now classified as a new species C. muridarum) was used for the study. Chlamydial growth in the lung was assessed by inoculating HeLa cell monolayer with lung homogenates followed by enzyme-linked immunosorbent assay (IFA). IL-17, IL-6 and MIP-2 were measured by enzyme-linked immunosorbent assay (ELISA). Mice without infection acted as the control group. In vitro, L929 cells were pretreated with recombinant murine IL-17 (rmIL-17) at a dose ranging from 20, 100 to 500 μg/L for 24 h then infected with MoPn for 24 h. The supernatants were harvested and tested for IL-6 and MIP-2 concentration using ELISA. The cells were assayed for the number of inclusion-forming unit (IFU) by IFA. L929 cells without pretreatment with rmIL-17 but infected with MoPn was the control group.
Results: The study showed that in vivo, Chlamydial growth in the lung was found on day 1 after infection, and reached its peak at day 8 (6.49±0.19, lg IFU/lung) with subsequent decline in quantity. IL-17 peaked at 48 h (83.0 ng/L±35.8 ng/L) while IL-6 peaked on day 3 [(3.98±0.04) μg/L], MIP-2 peaked on day 8 [(2.19±0.71) μg/L]. The study showed that in vitro, compared with control group [(55.10±16.54) ng/L for IL-6 production and (13.71±0.84) ng/L for MIP-2], L929 cells pretreated with rmIL-17 at the different concentrations of 20, 100 and 500 μg/L for 24 h then infected with MoPn for 24 h, could significantly increase IL-6 (P <0.01) and MIP-2 secretion (P <0.05). The productions of IL-6 in the supernatants were (531.65±24.40), (629.95±7.71), and (646.51±35.92) ng/L. Meanwhile, the productions of MIP-2 were (107.21±28.40), (181.95±25.51), and (221.90±17.32) ng/L, respectively. RmIL-17 alone had no effect on IL-6 and MIP-2 secretion, and no direct effect on growth of chlamydial inclusion body was demonstrated either.
Conclusion: IL-17 was produced early in airway upon Chlamydia trachomatis, and rmIL-17could induce IL-6 and MIP-2 production in L929 cells after infection with MoPn. These suggest that an early IL-17 response may play an important role by inducing the secretion of IL-6 and MIP-2 in initiating host defense against infection with Chlamydia trachomatis in the airway.