Objective   To evaluate the early IL-17 production in airway upon Chlamydia trachomatis infection and its relationship with chlamydial organism replication.   Methods   A total of 128 mice were randomly divided into experimental groups and control ones. The mice in experimental groups were induced by intranasal inoculation with Chlamydia trachomatis mouse pneumonitis (MoPn

now classified as a new species C. muridarum) biovar with 4000 IFU of MoPn. The same volume of SPG was given to the control ones. Chlamydial growth in the lung was assessed by inoculating HeLa cell monolayer with lung homogenates followed by IFA at 0

1

15

2

3

4

8 and 12 d after infection. Meanwhile

IL-17 was measured by ELISA. Another 24 mice were divided randomly into 3 groups and infected with 160

800

and 4 000 IFU of MoPn by intranasal inoculation

respectively. Chlamydial growth and IL-17 production in the lung were assessed at 2 d after infection. Another 16 mice were divided into experimental and control groups and were administrated with 4 000 IFU of MoPn by intranasal injection with or without rifampicin and chloromycepin treatment. Chlamydial growth and IL-17 production in the lung were also assessed at 2 d after infection.   Results   Chlamydial growth in the lung was found at 1 d after infection

and reached its peak at 8 d with subsequent decline in quantity. IL-17 peaked at 48 h transiently

and then decreased subsequently. Both Chlamydial growth and IL-17 production in the lung were detectable at 2 d after infection only with 4 000 IFU of MoPn by intranasal administration. Chlamydial growth in the lung was blocked by treatment with antibiotics. Meanwhile

no IL-17 was detectable by ELISA.    Conclusion   IL-17 can be produced early in airway upon Chlamydia trachomatis. IL-17 production may be associated with the dose of Chlamydia trachomatis infection and early chlamydial organism replication.