Abstract

OBJECTIVE: Under physiological conditions, scavenger receptors serve to scavenge or clean up cellular debris and other related materials, and they play a role in host defense. Considering the functional role of scavenger receptors in mediating phagocytosis, it is reasonable to hypothesize that the levels of scavenger receptors in peritoneal macrophages may play an important role in the pathogenesis of endometriosis.DESIGN: A prospective, experimental study.MATERIALS AND METHODS: To determine which factors are responsible for reduced phagocytosis, peritoneal macrophages were isolated from patients with or without endometriosis and the expression of several scavenger receptors was examined by RT-PCR. We further analyzed the expression in peritoneal macrophages isolated from control group, and women with early- and severe-stage endometriosis by real time RT-PCR, when the difference was significant.RESULTS: Preliminary data revealed that CD36, SR-AI, SR-AII, SR-BI, and SR-BII were expressed by peritoneal macrophages while SR-AIII was undetectable. By comparing the expression level of these scavenger receptors in normal and endometriosis peritoneal macrophages, level of CD 36 in macrophages isolated from endometriosis was lower than that from normal macrophage while levels of the other scavenger receptors mRNAs were not different. The results of real time RT-PCR further demonstrated that expression of CD36 in peritoneal macrophages isolated from women with endometriosis was less than that from normal women. Concordantly, the phagocytic ability of peritoneal macrophages isolated from women with endometriosis was weaker than those isolated from healthy women.CONCLUSIONS: The result clearly provides strong evidence to support our hypothesis that CD36 plays important role in phagocytosis and the pathological process of endometriosis. Further studies are warranted to investigate detail mechanisms of regulation of CD36 expression in peritoneal macrophages and its clinical implications in the development of endometriosis. OBJECTIVE: Under physiological conditions, scavenger receptors serve to scavenge or clean up cellular debris and other related materials, and they play a role in host defense. Considering the functional role of scavenger receptors in mediating phagocytosis, it is reasonable to hypothesize that the levels of scavenger receptors in peritoneal macrophages may play an important role in the pathogenesis of endometriosis. DESIGN: A prospective, experimental study. MATERIALS AND METHODS: To determine which factors are responsible for reduced phagocytosis, peritoneal macrophages were isolated from patients with or without endometriosis and the expression of several scavenger receptors was examined by RT-PCR. We further analyzed the expression in peritoneal macrophages isolated from control group, and women with early- and severe-stage endometriosis by real time RT-PCR, when the difference was significant. RESULTS: Preliminary data revealed that CD36, SR-AI, SR-AII, SR-BI, and SR-BII were expressed by peritoneal macrophages while SR-AIII was undetectable. By comparing the expression level of these scavenger receptors in normal and endometriosis peritoneal macrophages, level of CD 36 in macrophages isolated from endometriosis was lower than that from normal macrophage while levels of the other scavenger receptors mRNAs were not different. The results of real time RT-PCR further demonstrated that expression of CD36 in peritoneal macrophages isolated from women with endometriosis was less than that from normal women. Concordantly, the phagocytic ability of peritoneal macrophages isolated from women with endometriosis was weaker than those isolated from healthy women. CONCLUSIONS: The result clearly provides strong evidence to support our hypothesis that CD36 plays important role in phagocytosis and the pathological process of endometriosis. Further studies are warranted to investigate detail mechanisms of regulation of CD36 expression in peritoneal macrophages and its clinical implications in the development of endometriosis.

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