CONICET | Buscador de Institutos y Recursos Humanos

Chlamydia trachomatis is the causative bacterial agent of an increasing number of genital tract infections worldwide, annually. Although treatable with antibiotics, C. trachomatis infections are often asymptomatic, persistent and recurring; suggesting that infection does not induce a good protective immunity and those mechanisms that dampen the immune response may be involved. Using an in vivo male genital tract model of infection, we have previously demonstrated that the inoculation of NOD mice with Chlamydia muridarum in the meatus urethra results in an ascending and sustained infection. In the present work, we analyzed the pattern of cytokines secreted by spleen mononuclear cells (SMC) from infected or control NOD mice at different time post inoculation. Infected mice developed an ascending and sustained infection throughout the experimental schedule and mild leukocyte infiltration of prostate tissue. SMC from infected NOD mice incubated with polyclonal stimuli (Con A or anti CD3/CD28) secreted similar levels of IFNg or IL-17 but significantly higher amounts of IL-10 when compared to the values observed in SMC from control mice (p <0.0001). This higher production of IL-10 was observed at 7, 14 and 30 days post inoculation. When chlamydial antigen-specific IL-10 secretion was assessed, higher levels were also produced by SMC from infected NOD mice. Although chlamydial antigen-specific IL-10 levels secreted by SMC from control mice were lower than those from infected animals, they were significantly higher than those secreted by non-stimulated cells and in an antigen dose-dependent fashion. These results suggest that Chlamydia muridarum triggers an IL-10 biased immune response that may be involved in the chronic nature of this infection allowing bacterium persistence within the genital tract of the host.