Eutopic endometrium from patients with endometriosis modulates the expression of CD36 and SIRP‐α in peritoneal macrophages

Qi Xie, Hua He, Yahong Wu, Ya-Hong Wu, Lu-Jie Zou, Lu‐Jie Zou, Xiao-Ling She, Xiaoling She, Xiao-Meng Xia, Xiaomeng Xia, Xianqing Wu
Journal of Obstetrics and Gynaecology Research · 2019 · vol. 45(5) , pp. 1045–1057 · doi:10.1111/jog.13938 · PMID:30843336 · PMC6593754 · W2921968603
article OA: gold CC0 ⤵ 27 in-corpus citations
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⚙ AI-generated summary by claude@2026-06, 2026-06-08 ⓘ

Peritoneal macrophages from endometriosis patients showed altered SIRP-α and CD36 expression, with eutopic endometrium modulating these markers in vitro via NF-κB and TGF-β pathways.

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Abstract

AIM: This study aimed to investigate the in vitro alterations of the expression of signal regulatory protein-α (SIRP-α) and CD36 in macrophages in the endometriosis condition. METHODS: The expression of SIRP-α and CD36 was measured in peritoneal macrophages and peripheral blood mononuclear cells of endometriosis patients and control participants. The expressions of SIRP-α and CD36 were measured in human acute monocytic leukemia (THP-1) cell-derived macrophages that were treated with interleukin-6 (IL-6)-induced conditioned medium, eutopic versus normal endometrial homogenate, or lipopolysaccharide in the presence or absence of nuclear factor kappa-B (NF-κB) or transforming growth factor (TGF-β) inhibitors, respectively. RESULTS: Peritoneal macrophages that were isolated from women with endometriosis exhibited an enhanced expression of SIRP-α and a decreased expression of CD36 compared to control participants. Women with endometriosis had significantly higher levels of SIRP-α and CD36 in peripheral circulating mononuclear cells than in control participants. SIRP-α expression was significantly increased, whereas the CD36 expression was decreased in THP-1 cell-derived macrophages after treatment with eutopic endometrial homogenate. Intervention with IL-6-induced conditioned medium resulted in the downregulation of SIRP-α but the upregulation of CD36 in THP-1 cells. Incubation with the NF-κBp50 inhibitor decreased the expression of CD36 and SIRP-α in macrophages that were treated with normal endometrial homogenate, whereas the TGF-β inhibitor enhanced the CD36 expression of THP-1 cell-derived macrophages treated with eutopic endometrial homogenate. CONCLUSION: The eutopic endometrium could reduce the phagocytic ability of peritoneal macrophages in women with endometriosis through the modulation of SIRP-α and CD36 expression. Inhibition of the TGF-β signal pathway may be a potential therapeutic target for the treatment of endometriosis.

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Condition tags

endometriosis

MeSH descriptors

Antigens, Differentiation CD36 Antigens Endometriosis Macrophages, Peritoneal Receptors, Immunologic Antigens, Differentiation CD36 Antigens Endometriosis Female Humans Macrophages, Peritoneal Receptors, Immunologic THP-1 Cells

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