The presence of endometrial cells in the peritoneal cavity enhances monocyte recruitment and induces inflammatory cytokines in mice: Implications for endometriosis

Xuan Cao, Cao X, Yang D, Dongzi Yang, Song M, Mingqing Song, Murphy A, Ana Murphy, Ana A. Murphy, Sampath Parthasarathy, Parthasarathy S
Fertility and sterility · 2004 · vol. 82 , pp. 999–1007 · doi:10.1016/j.fertnstert.2004.04.040 · PMID:15474064 · W2074882515
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This study found that endometrial cells in the peritoneal cavity of mice promote monocyte recruitment and the release of inflammatory cytokines, suggesting a mechanism for endometriosis development.

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Abstract

ObjectiveTo determine the inflammatory response in the peritoneal cavity by the presence of endometrial cells and the role of the mesothelium.DesignIn vivo study using mice.SettingUniversity research laboratory.Animal(s)Female Swiss Webster mice, 8 to 10 weeks old.Intervention(s)Homogenous mouse endometrial epithelial and stromal cells were injected intraperitoneally. Peritoneal lavage and mesothelium were collected 4 to 72 hours after the administration.Main outcome measure(s)We determined the number of peritoneal macrophages, and the production and gene expression of monocyte chemotactic protein-1 (MCP-1/JE), interleukin 1alpha (IL-1alpha), and interleukin 6 (IL-6).Result(s)The intraperitoneal administration of endometrial cells increased the number of peritoneal macrophages, production of MCP-l, IL-1alpha, and IL-6, and expression of mesothelial MCP-1/JE, IL-1alpha, and IL-6 genes in recipient mice.Conclusion(s)These results suggest that retrograde menstruation could account for the increased presence of inflammatory mediators in the peritoneal cavity of women with endometriosis. The mesothelium could play an active role in endometriosis in addition to providing an attachment stratum for the endometrial cells.

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Condition tags

endometriosis

MeSH descriptors

Cytokines Endometrium Inflammation Mediators Monocytes Peritoneal Cavity Peritoneal Cavity Animals Chemokine CCL2 Chemokine CCL2 Chemokine CCL2 Cytokines Endometriosis Endometriosis Endometrium Epithelial Cells Epithelial Cells Female Gene Expression Regulation Inflammation Mediators Interleukin-1

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