Resolution of chlamydial genital infection in B-cell-deficient mice and immunity to reinfection

Abstract

The purpose of this investigation was to determine the relative roles of the humoral and cell-mediated immune responses in the resolution of chlamydial genital infection of mice and resistance to reinfection. To this end, female BALB/c mice were rendered B cell deficient by treatment with heterologous anti-immunoglobulin M (IgM) serum from birth. Controls were similarly treated with either normal serum or phosphate-buffered saline. Before inclusion in each experiment, aiti-IgM-treated mice were screened for the absence of IgM in serum and for the presence of cell-mediated immune responses. In addition, ppleen cells from anti-IgM-treated mice responded to concanavalin A and phytohemagglutinin but not to lipopolysaccharide. By these criteria, mice were designated B cell deficient. B-cell-deficient mice and controls were inoculated intravaginally with a suspension of mouse pnecvumonitis agent (MoPn), a Chiamydia trachomatis biovar. All B-cell-deficient mice resolved the infection. Additionally, no significant difference was seen in the course of the infection in B-cell-deficient mice when compared with controls. In contrast to control mice, B-cell-deficient mice displayed no detectable antibody responses to MoPn in serum or in genital secretions. However, both B-cell-deficient mice and controls developed delayed-type hypersensitivity and T-cell proliferative responses to MoPn. When challenged 53 days after primary infection, no significant difference was seen in the resistance of B-cell-deficient mice to reinfection when compared with that of the controls. These data indicate that cell-mediated immune mechanisms play an important role in the resolution of and resistance to chlamydial genital infection in this model.

Immunological memory in B‐cell‐deficient mice conveys long‐lasting protection against genital tract infection with Chlamydia trachomatis by rapid recruitment of T cells

“…This ®nding is in agreement with previous studies demonstrating that local antibodies play a subordinate role also in short-term anti-chlamydial protection. 11,14,15 Somewhat at variance with the present study, Su et al reported that mMT mice were more susceptible to reinfection than were WT mice, at 70 days following a primary infection. Of note, we observed that clearing of the transient local infection was delayed in some of the memory mMT mice, but not in the WT mice, which may indicate that antibodies can in¯uence the course of the transient infection.…”

AVibrio choleraeghost-based subunit vaccine induces cross-protective chlamydial immunity that is enhanced by CTA2B, the nontoxic derivative of cholera toxin

“…After the challenge, mice were observed twice daily for clinical signs of adverse reaction to infection. To assess the level of infection, cervicovaginal swabs were collected from each animal every 3 days following the challenge and C. muridarum was isolated from swabs in tissue culture by standard methods (Ramsey et al, 1988). The experiment was repeated to contain 12-15 mice per group.…”

Blockade of epithelial membrane protein 2 (EMP2) abrogates infection ofChlamydia muridarummurine genital infection model

“…Chlamydia muridarum was used as purified infectious elementary bodies (Ramsey et al, 1988) or inactivated by UV irradiation as previously described (Caldwell et al, 1981).…”