Immunological aspects of genital chlamydia infections.

Overview

Chlamydia trachomatis ascends from the cervix to the Fallopian tubes where it forms a persistent infection. The immune response to this infection results in tubal occlusion and infertility. In its persistent formC. trachomatis produces high levels of a 60-kDa heat shock protein (c-hsp60). There is a human hsp60 (h-hsp60) which shares a 50% amino acid sequence homology with the c-hsp60. Therefore, a chlamydial Fallopian tube infection can induce the development of autoantibodies to h-hsp60. H-hsp60 is one of the first proteins synthesized following fertilization. It is also expressed by epithelial cells in the decidua. Therefore, expression of h-hsp60 in early pregnancy can reactivate the c-hsp60-sensitized lymphocytes, leading to immune rejection of the embryo. The role of C. trachomatis in male infertility requires clarification. Because most C. trachomatis infections occur without defined symptoms, only the screening of sexually active women will reveal whether a woman is infected with this organism. Detection and treatment of a recently acquired infection can prevent development of h-hsp60 autoantibodies and tubal occlusion, preserve fertility, and prevent complications such as ectopic pregnancy.