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

被引：78

作者：

PATTON, DL ^{[1
]}

SWEENEY, YTC ^{[1
]}

KUO, CC ^{[1
]}

机构：

[1] UNIV WASHINGTON,DEPT PATHOBIOL,SEATTLE,WA 98195

来源：

JOURNAL OF INFECTIOUS DISEASES | 1994年 / 169卷 / 03期

关键词：

D O I：

10.1093/infdis/169.3.680

中图分类号：

R392 [医学免疫学]; Q939.91 [免疫学];

学科分类号：

100102 ;

摘要：

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

引用

页码：680 / 683

页数：4

共 13 条

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[2]

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[3]

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