C1q is responsible of the anti-inflammatory behavior of decidual endothelial cells

PROBLEM: Endothelial cells (ECs), although similar in function and morphology, represent an heterogeneous population of cells in terms of secretion of inflammatory mediators, modulation of adhesion molecules, leakiness and pro-coagulant activity and play a fundamental role in the control of the inflammatory response. Excessive inflammation at foetal-maternal interface is thought to be a key contributor in a compromised pregnancy. Intrauterine infections have been associated with pregnancy complications such as preterm labor, intrauterine growth restriction and preeclampsia. We demonstrated that decidual endothelial cells (DECs) compared to ECs isolated from adult skin (ADMECs) are ipo-responsive to the pro-inflammatory stimulus LPS for the expression of adhesion molecules and cytokines secretion. We showed also that DECs express lower level of TLR4, MD2 and MyD88 compared to ADMECs and this may be important for the control of the inflammatory response at foeto-maternal interface. We have previously shown that DECs acquired the ability to synthesize C1q during pregnancy which is to a large extent localized on the cell surface. Since it has been demonstrated that C1q suppressed LPS-induced IL-12p40 production in bone marrow-derived DC (BMDC) we hypothesised that C1q can play a role in the control of DECs response to LPS. METHODS: We investigated the expression of TLR4, MD-2, and MyD88 in ADMECs previously incubated for two hours with C1q in cells stimulated or not with LPS by Real Time PCR, Western blotting and cytofluorimetric analysis. RESULTS: Our results showed that C1q affects mRNA expression of TLR4, MD-2, and MyD88 both in resting and in stimulated cells, CONCLUSION: The presence of C1q at foeto maternal interface may be responsible of the control of inflammation during pregnancy.