Inhibition of CD36-Dependent Phagocytosis by Prostaglandin E2 Contributes to the Development of Endometriosis

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Prostaglandin E2 inhibits CD36-dependent phagocytosis, a process that contributes to the development of endometriosis.

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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) E(2), via the EP2 receptor-dependent signaling pathway, inhibits the expression of CD36 in peritoneal macrophages, resulting in reduced phagocytic ability. PGE(2)-mediated inhibition of macrophage phagocytic capability was restored by ectopic expression of CD36. Treatment with PGE(2) inhibited CD36-dependent phagocytosis of peritoneal macrophages and increased the number and size of endometriotic lesions in mice. In contrast, blockade of PGE(2) 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.

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Condition tags

endometriosis

MeSH descriptors

CD36 Antigens Dinoprostone Endometriosis Peritoneal Diseases Phagocytosis Phagocytosis Phagocytosis Phagocytosis Animals CD36 Antigens CD36 Antigens CD36 Antigens Cells, Cultured Dinoprostone Dinoprostone Down-Regulation Down-Regulation Endometriosis Endometriosis Endometriosis

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europepmc
last seen: 2026-08-04T06:16:37.499272+00:00
openalex
last seen: 2026-06-10T17:14:06.276822+00:00
pubmed
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