Prior Genital Tract Infection with a Murine or Human Biovar of Chlamydia trachomatis Protects Mice against Heterotypic Challenge Infection

We sought to assess the degree of cross-protective immunity in a mouse model of chlamydial genital tract infection. Following resolution of genital infection with the mouse pneumonitis (MoPn) biovar of Chlamydia trachomatis, mice were challenged intravaginally with either MoPn or human serovar E or L2. The majority of animals previously infected with MoPn were solidly immune to challenge with either of the two human biovars. Surprisingly, approximately 50% of animals became reinfected when homologously challenged with MoPn, although the secondary infection yielded significantly lower numbers of the organism isolated over a shorter duration than in the primary infection. Primary infection with serovar E also protected against challenge with MoPn or serovar L2, although the degree of immune protection was lower than that resulting from primary infection with MoPn. Blast transformation and assessment of delayed-type hypersensitivity indicated that mice previously infected with either human or murine biovars produced broadly cross-reactive T cells that recognized epitopes of either murine or human biovars of C. trachomatis. Immunoblotting demonstrated that primary MoPn infection produced immunoglobulin G (IgG) antibody to antigens of MoPn as well as at least three distinct antigenic components of human serovar E, one of which was identical in molecular weight to the major outer membrane protein (MOMP). Primary infection with serovar E produced IgG antibody reactive against serovar E but not MoPn MOMP and against at least one ca. 60-kDa protein of both chlamydial strains. Our results indicate that primary genital infection of mice with murine C. trachomatis induces immunity against challenge with either of two human biovars.

本研究旨在评估沙眼衣原体生殖道感染小鼠模型中的交叉保护性免疫水平。在小鼠经沙眼衣原体小鼠肺炎（Mouse Pneumonitis, MoPn）生物型感染生殖道并清除感染后，对其分别经阴道途径攻击接种MoPn、人源血清型E（serovar E）或L2（serovar L2）衣原体。既往感染MoPn的大多数小鼠，对两种人源生物型的攻击感染均呈现完全免疫。令人意外的是，当用MoPn进行同源攻击感染时，约50%的小鼠发生再次感染；尽管与初次感染相比，二次感染的病原体分离载量显著更低，且持续时间更短。经血清型E初次感染的小鼠，同样可抵御MoPn或血清型L2的攻击感染，但其免疫保护水平低于MoPn初次感染所诱导的保护效果。淋巴母细胞转化实验与迟发型超敏反应检测结果显示，既往感染人源或鼠源生物型沙眼衣原体（C. trachomatis）的小鼠，均可产生广泛交叉反应性T细胞，这些T细胞可识别鼠源或人源生物型沙眼衣原体的抗原表位。免疫印迹（Immunoblotting）实验结果表明，MoPn初次感染可诱导产生针对MoPn抗原的免疫球蛋白G（Immunoglobulin G, IgG）抗体，同时也可识别至少3种人源血清型E衣原体的独特抗原组分，其中一种组分的分子量与主要外膜蛋白（Major Outer Membrane Protein, MOMP）一致。血清型E初次感染则可诱导产生针对血清型E的IgG抗体，无法识别MoPn的MOMP，但可识别两种衣原体菌株共有的至少1种约60 kDa的蛋白。本研究结果证实，小鼠经鼠源沙眼衣原体初次感染生殖道后，可诱导产生抵御两种人源生物型衣原体攻击感染的免疫能力。