Abstract:[Objective] To determine the cause of Chlamydia muridarum-induced pathology in urogenital tract of mice with various genetic background, and to explore the mechanism of inflammatory cells’ dynamic changes in pathological difference of mice infected with chlamydia. [Methods] Each of DBA/2J and A/J mice was inoculated via intrauterine route with 2×105 inclusion forming units (IFUs) of live C. muridarum organisms. Mice were sacrificed on 60 days post infection, and the severity of oviduct hydrosalpinx from each mouse was examined visually. The severity of inflammation and pathologies were scored under microscope. Vaginal swabs were taken on 3, 7, 14, 21, 28, 35, 42, 49, 56 and 60 days post infection from each group of mice and the total number of IFUs per swab was calculated. Five mice per group were sacrificed on 14 days post infection, each section of urogenital tract was made into homogenates for measuring the number of IFUs and the level of cytokines per sample. Meanwhile, 5 mice per group were sacrificed each time on 3, 28 and 35 dpi for diagnosis of the type and dynamic changes of inflammatory cells in the diseased tissues. [Results] Two groups of mice had statistically significant differences in hydrosalpinx incidence and severity of dilation whereas no statistically difference in the scores for the severity of inflammation. DBA/2J and A/J mice displayed same in number of chlamydial IFUs and pathology positive mice rate. The level of some inflammatory cytokines but not the number of IFUs detected in oviduct and ovary homogenate on 14 days had statistically difference. In early stage of infection neutrophils in pathological tissues increased in both DBA/2J and A/J mice whereas no obvious difference in two results. Many eosinophils occurred in pathological tissues of DBA/2J mice on 28 days and displayed statistically difference with A/J mice on 35 days. [Conclusion] The pathological difference of urogenital tract from DBA/2J and A/J mice with intrauterine inoculation of C. muridarum may have relationship with eosinophils-involved inflammatory reaction.