DEMONSTRATION OF DELAYED-HYPERSENSITIVITY IN CHLAMYDIA-TRACHOMATIS SALPINGITIS IN MONKEYS - A PATHOGENIC MECHANISM OF TUBAL DAMAGE

The role of delayed hypersensitivity in the pathogenesis of Chlamydia trachomatis salpingitis was studied in the monkey ''pocket'' model. Pi gtailed monkeys (Macaca nemestrina) were sensitized by inoculation of live C. trachomatis organisms (E/UW-5/Cx) into subcutaneous pockets co ntaining salpingeal autotransplants. At 21 days, affinity-purified rec ombinant C. trachomatis heat-shock protein (rhsp60) was injected into pockets either previously sensitized with C. trachomatis or not sensit ized in the same monkey. Delayed-type hypersensitivity reaction was ob served, characterized by mononuclear cell infiltration with peak react ion at 48 h. Injection of rhsp60 into the pockets of a naive animal di d not induce inflammation. This study showed that C. trachomatis infec tion in monkeys induced delayed hypersensitivity, which is mediated by hsp60. Histologic findings of the salpinx were consistent with delaye d hypersensitivity reaction observed in ocular C. trachomatis infectio n, further suggesting a similar pathogenesis for both salpingitis and trachoma.