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Mast Cell-Mediated Remodeling and Fibrinolytic Activity Protect against Fatal Glomerulonephritis¹

Yutaka Kanamaru^2,*, Lisa Scandiuzzi^2,*, Marie Essig^*, Cristiana Brochetta^*, Claudine Guérin-Marchand^*, Yasuhiko Tomino, Renato C. Monteiro^*, Michel Peuchmaur and Ulrich Blank^3,*

^* Institut National de la Santé et de la Recherche Médicale Unité 699, Bichat Medical School, Paris, France; Division of Nephrology, Department of Internal Medicine, Jutendo University, School of Medicine, Tokyo, Japan; and Service de Pathologie, Hôpital Robert Debré, Assistance Publique-Hôpitaux de Paris, Establissement Associé 3102, and Université Paris 7, Paris, France

Mast cells are detrimental in several inflammatory diseases; however, their physiological roles are also increasingly recognized. Recent data suggest that mast cells may also be involved in renal diseases. We therefore used congenitally mast cell-deficient W/W^v mice and normal +/+ littermates to assess their role in anti-glomerular basement membrane-induced glomerulonephritis. Following administration of anti-glomerular basement membrane Abs, W/W^v mice exhibited increased mortality as compared with +/+ mice owing to rapid deterioration of renal function. Reconstitution of the mast cell population in W/W^v mice restored protection. This was independent of activating FcR, as protection was also obtained using mast cells deficient in FcR. Comparative histological analysis of kidneys showed that deterioration of renal function was caused by the presence of thick layers of subendothelial glomerular deposits in W/W^v mice, while +/+ mice or mast cell-reconstituted W/W^v mice showed significantly less. Deposits appeared during the early phase of disease and persisted thereafter, and were accompanied by enhanced macrophage recruitment. Immunohistochemical analysis revealed increased amounts of fibrin and type I collagen in W/W^v mice, which were also unable to maintain high tissue plasminogen activator and urinary-type plasminogen activator activity in urine in the heterologous phase of disease. Our results indicate that mast cells by their ability to mediate remodeling and repair functions are protective in immune complex-mediated glomerulonephritis.

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				K. Hochegger, A. R. Rosenkranz, F. Siebenhaar, and M. Maurer Comment on "Mast Cell-Mediated Remodeling and Fibrinolytic Activity Protect against Fatal Glomerulonephritis" J. Immunol., August 1, 2006; 177(3): 1377 - 1377. [Full Text] [PDF]

				Y. Kanamaru, L. Scandiuzzi, M. Essig, R. C. Monteiro, and U. Blank Response to Comment on "Mast Cell-Mediated Remodeling and Fibrinolytic Activity Protect against Fatal Glomerulonephritis" J. Immunol., August 1, 2006; 177(3): 1377 - 1378. [Full Text] [PDF]