Integrin-mediated adhesion of uterine endometrial cells from endometriosis patients to extracellular matrix proteins is enhanced by tumor necrosis factor alpha (TNFα) and interleukin-1 (IL-1)
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TNFα and IL-1 significantly increase the adhesion of uterine endometrial cells from endometriosis patients to extracellular matrix proteins, suggesting a role in disease pathogenesis.
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Abstract
Objectives(1) to demonstrate specificity of integrin function in endometrial cell adhesion; (2) to investigate their regulation by tumor necrosis factor alpha (TNF alpha) and interleukin-1 (IL-1); and (3) to detect differences between cells from patients with and without endometriosis.Study designEndometrial cell cultures from ten patients with and 13 without endometriosis were tested for their expression of integrins alpha2beta1, alpha5beta1, alpha(v)beta3, and alpha4beta1 by immunocytochemistry and for their adhesion to collagen type IV, laminin, and fibronectin.ResultsIntegrin expression was independent of cytokine treatment. Addition of antiintegrin antibodies inhibited adhesion. A significant increase in adhesion to laminin and fibronectin was seen in endometriosis after IL-1 treatment and additionally to collagen after TNF alpha. Cells from women without endometriosis showed a significant increase only to fibronectin.ConclusionsHuman endometrial cells express functional integrins in vitro. TNF alpha and IL-1 had more pronounced effects on adhesion in endometriosis. Inflammatory cytokines in the peritoneal cavity may facilitate adhesion of retrogradely menstruated endometrial fragments in endometriosis.
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