[Role of LIGHT signal pathway in Chlamydia muridarum urogenital infection in mice].

Objective: To study the role of lymphotoxin-like inducible protein that competes with glycoprotein D for herpesvirus entry on T cells (LIGHT) in the development of protective immunity and pathology during Chlamydia Muridarum urogenital infection in mice.

Methods: C57BL/6J wild type (wt) and mice deficient in LIGHT (LIGHT KO) were inoculated intravaginally with 1 x 10(4) IFUs of live C. muridarum organisms. Half mice of each group were reinfected on day 49 after primary infection. We took mice vaginal swabs every 3 or 4 days to monitor live organism shedding. On day 80 after the primary infection, mice were sacrificed, the vaginal tract was isolated for pathology analysis. The spleen cells were collected and IL-4, IL-5, IL-17 and IFN-y were detected by ELISA in the spleen cells culture supernatant after restimulated by UV-MoPn EB. The titers of different Ab isotypes were measured in mice serum by Indirect Immunofluorescence Assay.

Results: The chlamydia shedding time of LIGHT KO mice was similar to wild type mice, which cleared the organisms within 28 days after primary infection, and acquired protective immunity against C. muridarum reinfection. All mice regardless of genotypes developed severe upper genital tract pathology and showed no significant difference between LIGHT KO and wild type mice. All mice developed robust anti-C. muridarum organism IgG antibody responses and the ratios of IgG2a versus IgG1 showed no significant difference between LIGHT KO and wild type mice. Splenocytes from MoPn-infected LIGHT KO and wild type mice produced high levels of IFN-gamma and IL-17, but IL-4 and IL-5 couldn't be detected.

Conclusions: LIGHT signal pathway may not correlated with protection against C. muridarum urogenital tract infection and urogenital tract pathology induced by C. muridarum.