Chlamydial Heat Shock Protein 60 And Immunopathogensis

Chlamydial genital infection is one of sexually transmitted dieases, which endangers the reproductive health of women worldwide. In the United States, It is estimated that 4 million cases occur annually, and 50,000 women a year become infertile as a result of chlamydial infection. The incidence of chlamydial diseases are increasing gradually,20 -30% patients with STD are infected by CT. Chlamydial genital infections include cervicitis, pelvic inflammatory disease, ectopic pregnancy and infertility. The asymptomatic and persistent character of chlamydial infections can lead to the infection spreading and cause a major public health problem to the reproductive heath of women in developed and developing countries. Up to now, the mechanism of chlamydial infection is not entirely understood. The immunologic response to C. trachomatis infection is considered as a fundamental mechanisim for chronic chlamydial infection of female reproductive tract. Chsp60 plays a major role in inducing CT infection sequelae.The C. trachomatis hsp60, a potential component of the cellular outer membrane , involved in membreane reorganization, may play an important role in the induction of either immunopathological or protective immune response. At the beginning of 1990 s, a chlamydial component present in the Triton X -100 - soluble fraction of chlamydia EBs has been reported to induce ocular hypersensitive responses in previously infected animal. The predominant antigenic component present in the Triton X -100 - soluble fraction was shown to be a protein of approximately 60,000 molecular weight. Boviol et al found that the Triton X - 100 - soluble 60,000 molecular weight protein of C. trachomatis was antigenically i-dentical to the hsp60 family. Monkeys previously infected with CT developed se-vere conjunctival inflammation, the delayed type hypersensitivity are responsible for tissue damage. Serological responsiveness to chsp60 is correlated with the severe sequelae such as ectopic pregnancy and infertility in human chlamydial infection. These study strongly implicated the immune response to the chlamydial hsp60 as a contributing factor in the pathogenesis of chlamydial disease and chlamydial chronic inflammatory diseases.These previous studies suggested that reinfection and the host's immune response be important factors in immunopathogenesis to C. trachomatis. Chsp60 antibody response may be a marker for persistent or repeated chlamydial infection. Repeated cervical chlamydial infection has been identified as a risk factor for human PID. T cell response and the chsp60 antibody response may mediate the inflammatory pathological injury in C. trachomatis PID. Because chsp60 are highly conserved, and 48% homology with hsp60 of other procarytes and euca-ryotes. Hsp60 antibody response to chsp60 may be a marker of autoimmune responses initiated by cross - reactivity between chsp60 epitopes and host - cell hsp60 epitopes, and autoimmunological disease was elicited. A recent study showed antecedent antibody response to chsp60 predicted a 2 to 3 fold increased risk of develoment of human PID, suggesting that chsp60 itself may be a causal factor in the immunopathogenesis of chlamydial disease. Purified recombinant cshp60 has also been shown to cause pathology suggestion of a delayed type hypersensitivity response in a primate model of salpingitis. A number of studies have shown that high levels of serum antibody to this chlamydial heat shock protein associated with the develoment of adverse reproductive sequelae following genital chlamydial infection. If chsp60 gene can be cloned and purified, a more complete understanding of the immune responses elicited by these conserved proteins will provide information concerning its role in the pathogenesis of chlamydial disease.Antibody responses to chsp60 may be correlated with self - reactive B cell or genetic factor. One intriguing observation is that in mice, antibody responses to chsp60 are genetically determined, in part , by genes located within the major histocompatibility complex...