Influence of TH1/TH2 switched immune response on renal ischemia-reperfusion injury
Nenhuma Miniatura disponível
Data
2006-01-01
Autores
Marques, Vilmar Paiva [UNIFESP]
Gonçalves, Giselle Martins [UNIFESP]
Feitoza, Carla Quarin [UNIFESP]
Cenedeze, Marcos Antonio [UNIFESP]
Bertocchi, Ana Paula Fernandes [UNIFESP]
Damiao, Marcio Jose [UNIFESP]
Pinheiro, Helady Sanders
Teixeira, Vicente Paula Antunes
Reis, Marlene Antonia dos
Pacheco-Silva, Alvaro [UNIFESP]
Orientadores
Tipo
Resenha
Título da Revista
ISSN da Revista
Título de Volume
Resumo
Background/Aims: Recent evidence shows a critical role of the CD4+ T cell with the Th1/Th2 paradigm as a possible effector mechanism in ischemia and reperfusion injury. We hypothesize that a polarized Th1 activation response may negatively influence the renal IRI through its relationship with chemokine production (MCP-1) and with a protective tissue response (HO-1). Methods: We subjected mice to renal ischemia for 45 min using IL-4 and IL-12 knockout C57BL/6. We then measured serum urea levels, performed histomorphometric analysis for tubular necrosis and regeneration, and evaluated the mRNA expression of HO-1, t-bet, Gata-3 and MCP-1 by real-time PCR at 24,48 and 120 h after surgery. Results/Conclusions: the IL-4 knockout mice had a statistically significant rise in serum urea levels post IRI compared with control animals. the IL-12-deficient mice were not affected. the IL-4-deficient mice had a statistically significant increase in tubular injury and impairment in cell regeneration. the IRI in IL-4-deficient mice was accompanied by higher levels of HO-1, t-bet and later up-regulation of MCP-1. These findings suggest that the deleterious effects of the Th1 cell involve increased production of chemokines such as MCP-1. Copyright (c) 2006 S. Karger AG, Basel.
Descrição
Citação
Nephron Experimental Nephrology. Basel: Karger, v. 104, n. 1, p. E48-E56, 2006.