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Magnesium Research

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Effect of Mg-deficiency on endothelial cell allogeneic activation in a model of isolated perfused mouse lung Volume 18, numéro 4, december 2005

Auteurs
CNRS UMR 8078, IPSC, Université Paris-Sud 11, Centre Chirurgical Marie-Lannelongue, 133, avenue de la Résistance, 92350 Le Plessis Robinson, France, Faculté de Pharmacie, Université Paris-Sud 11, 92296 Châtenay-Malabry Cedex, France

Following vascularized organ allotransplantation, an early intragraft inflammatory process is initiated by adhesion molecule-ligand interaction between recipient blood leukocytes and graft endothelial cells (EC). We have previously shown that chronic hypomagnesemia did not induce any inflammatory process in the lung, hence neither EC activation, nor lung remodelling. In the present study we have investigated the effects of allogeneic blood perfusion on lungs from magnesium-deficient mice in our experimental model of isolated mouse lung. After 3h of isogeneic or allogeneic perfusion, no inflammatory process was detected by histochemical examination of lung tissue; the mRNA levels of the adhesion molecules E-selectin, ICAM-1 and VCAM-1, and of the pro-inflammatory cytokines TNF-α and IL-2 in lung tissue, determined by reverse transcriptase-polymerase chain reaction (RT-PCR), were similar, and the expression of E-selectin and I-A b antigen on EC by immunohistochemical staining was undetectable. All of these markers were shown to be dramatically increased after allogeneic perfusion of lung from magnesium-non deficient mice. Our results clearly show that allogeneic perfusion of lungs from magnesium-deficient mice cannot induce EC activation or lung inflammation, indicating that hypomagnesemia in donors does not constitute an additional risk for allograft outcome and might allow to lighten the recipient’s immunosuppressive treatment.