Inhibition of CD36-dependent phagocytosis by prostaglandin E2 contributes to the development of endometriosis

Pei Chin Chuang, Yiu Juian Lin, Meng Hsing Wu, Lih Yuh C. Wing, Yutaka Shoji, Shaw Jenq Tsai

Research output: Contribution to journalArticlepeer-review

66 Citations (Scopus)

Abstract

Dysfunction in macrophage-mediated phagocytosis of aberrant cells that undergo retrograde transport to the peritoneal cavity is considered an important factor in the development of endometriosis. However, the mechanisms responsible for the loss of function of macrophages remain largely unknown. Herein, we report that prostaglandin (PG) E2, via the EP2 receptor-dependent signaling pathway, inhibits the expression of CD36 in peritoneal macrophages, resulting in reduced phagocytic ability. PGE2-mediated inhibition of macrophage phagocytic capability was restored by ectopic expression of CD36. Treatment with PGE2 inhibited CD36-dependent phagocytosis of peritoneal macrophages and increased the number and size of endometriotic lesions in mice. In contrast , blockade of PGE2 production by cyclooxygenase inhibitors enhanced the phagocytic ability of peritoneal macrophages and reduced endometriotic lesion formation. Taken together, our findings reveal a potential mechanism of immune dysfunction during endometriosis development and may contribute to the design of an effective prevention/treatment regimen.

Original languageEnglish
Pages (from-to)850-860
Number of pages11
JournalAmerican Journal of Pathology
Volume176
Issue number2
DOIs
Publication statusPublished - 2010 Feb

All Science Journal Classification (ASJC) codes

  • Pathology and Forensic Medicine

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