Lung inflammation is induced by renal ischemia and reperfusion injury as part of the systemic inflammatory syndrome

Autor(es):Mostrar menos -

Campanholle, G. ^[1] ; Landgraf, R. G. ^[2] ; Goncalves, G. M. ^[1] ; Paiva, V. N. ^[1] ; Martins, J. O. ^[3] ; Wang, P. H. M. ^[4] ; Monteiro, R. M. M. ^[4] ; Silva, R. C. ^[4] ; Cenedeze, M. A. ^[4] ; Teixeira, V. P. A. ^[5] ; Reis, M. A. ^[5] ; Pacheco-Silva, A. ^[4] ; Jancar, S. ^[3] ; Saraiva Camara, Niels Olsen ^{[4, 1]}

Afiliação do(s) autor(es)

^[1] Univ Sao Paulo, Inst Biomed Sci 4, Dept Immunol, Lab Transplantat Immunobiol, BR-05508900 Sao Paulo - Brazil

^[2] Univ Fed Sao Paulo, Dept Biol Sci, Diadema - Brazil

^[3] Univ Sao Paulo, Inst Biomed Sci 4, Dept Immunol, Lab Immunopharmacol, BR-05508900 Sao Paulo - Brazil

^[4] Univ Fed Sao Paulo, Div Nephrol, Lab Clin & Expt Immunol, Sao Paulo - Brazil

^[5] Univ Fed Triangulo Mineiro, Dept Pathol, Uberaba, MG - Brazil

• Tipo de documento: Artigo Científico
• Fonte: Inflammation Research; v. 59, n. 10, p. 861-869, OCT 2010.
• Citações Web of Science: 17

Resumo

Ischemia and reperfusion injury (IRI) are mainly caused by leukocyte activation, endothelial dysfunction and production of reactive oxygen species. Moreover, IRI can lead to a systemic response affecting distant organs, such as the lungs. The objective was to study the pulmonary inflammatory systemic response after renal IRI. Male C57Bl/6 mice were subjected to 45 min of bilateral renal ischemia, followed by 4, 6, 12, 24 and 48 h of reperfusion. Blood was collected to measure serum creatinine and cytokine concentrations. Bronchoalveolar lavage fluid (BALF) was collected to determine the number of cells and PGE(2) concentration. Expressions of iNOS and COX-2 in lung were determined by Western blot. Gene analyses were quantified by real time PCR. Serum creatinine increased in the IRI group compared to sham mainly at 24 h after IRI (2.57 +/- A 0.16 vs. 0.43 +/- A 0.07, p < 0.01). The total number of cells in BAL fluid was higher in the IRI group in comparison with sham, 12 h (100 x 10(4) +/- A 15.63 vs. 18.1x10(4) +/- A 10.5, p < 0.05) 24 h (124 x 10(4) +/- A 8.94 vs. 23.2x10(4) +/- A 3.5, p < 0.05) and 48 h (79 x 10(4) +/- A 15.72 vs. 22.2 x 10(4) +/- A 4.2, p < 0.05), mainly by mononuclear cells and neutrophils. Pulmonary COX-2 and iNOS were up-regulated in the IRI group. TNF-alpha, IL-1 beta, MCP-1, KC and IL-6 mRNA expression were up-regulated in kidney and lungs 24 h after renal IRI. ICAM-1 mRNA was up-regulated in lungs 24 h after renal IRI. Serum TNF-alpha, IL-1 beta and MCP-1 and BALF PGE(2) concentrations were increased 24 h after renal IRI. Renal IRI induces an increase of cellular infiltration, up-regulation of COX-2, iNOS and ICAM-1, enhanced chemokine expression and a Th1 cytokine profile in lung demonstrating that the inflammatory response is indeed systemic, possibly leading to an amplification of renal injury. (AU)

• Processo FAPESP: 06/06236-2 - Papel dos receptores da bradicinina nos danos teciduais extra-renais desencadeados pela lesão de isquemia e reperfusão renal: estudo da ação citoprotetora da biliverdina
• Beneficiário: Gabriela Campanholle
• Modalidade de apoio: Bolsas no Brasil - Doutorado Direto
• Processo FAPESP: 07/07139-3 - Investigando o papel da heme-oxigenase 1 em diferentes processos inflamatórios renais em modelos animais
• Beneficiário: Niels Olsen Saraiva Câmara
• Modalidade de apoio: Auxílio à Pesquisa - Temático
• Processo FAPESP: 06/03982-5 - Aspectos moleculares envolvidos na atividade microbicida e inflamatória de leucócitos no pulmão
• Beneficiário: Sônia Jancar
• Modalidade de apoio: Auxílio à Pesquisa - Temático