Objective:To study the virulence of Chlamydia trachomatis(Ct)plasmid in a neonatal mice model of pneumonia induced by Ct. Methods:Forty-eight neonatal BALB/c mice were randomly divided into four groups(each n=9)within 24 h after birth: wild type(WT)group(infected with Ct serovar D wild type)

plasmid free type(PF)group(infected with Ct serovar D plasmid free type)

phosphate buffer(PBS)group and normal group. Four mice in each group were sacrificed on 4

7

11 days. The lung tissue was collected for pathological analysis and counts of neutrophils infiltration. The expression of omp A gene

level of tumor necrosis factor-α and interferon-γ were determined by RT-PCR and ELISA assays respectively. Activation of TLR2 and NF-κB was tested by SEAP reporter assays.Results:Ct collected from homogenates was negative whereas omp A m RNA was detected in infection groups. The mice infected with PF strain had obvious pathological changes with neutrophils infiltration(1.10±0.19)and(21.06±10.92)

respectively

both decreased significantly than those of WT-infected mice(1.44 ±0.17) and(43.90±17.17)

respectively(P=0.048

0.005). The secretion of TNF-α and IFN-γ in the lung was obviously increased in WT-infected mice(623.35 ±37.23) and(2206.83 ±854.22)

respectively

than in non-infection mice(470.93 ±20.83) and(737.97±79.89)(P=0.000

0.038)

respectively. There was no statistic difference in TNF-α and IFN-γ secretion between PF-infected mice(531.59±34.14)and(1 099.86±427.39)

respectively and non-infected mice in control group(P >0.05). In addition

PF strain can activate TLR2(F =483.199

P =0.000)

but its intensity was lower than WT strain in vitro(P=0.000). NF-κB activation was restricted in PF strain

and there was no significant difference between control group and PF group in this regard(F=229.884

P=1.000). Conclusion:Plasmid-deficient Ct exhibits attenuated virulence in lung infection of neonatal mice

which may relate with down-regulated activation of NF-κB and TLR2 due to unknown factor of Chlamydia plasmid.