Lung inflammation is induced by renal ischemia and reperfusion injury as part of the systemic inflammatory syndrome
Contribuinte(s) |
UNIVERSIDADE DE SÃO PAULO |
---|---|
Data(s) |
20/10/2012
20/10/2012
2010
|
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. Desenvolvimento Cientifiproco e Tecnologico (CNPq) Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq) Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP) FAPESP[06/06236-2] Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP) FAPESP[06/03982-5] Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP) FAPESP[07/07139-3] |
Identificador |
INFLAMMATION RESEARCH, v.59, n.10, p.861-869, 2010 1023-3830 http://producao.usp.br/handle/BDPI/28263 10.1007/s00011-010-0198-0 |
Idioma(s) |
eng |
Publicador |
SPRINGER BASEL AG |
Relação |
Inflammation Research |
Direitos |
restrictedAccess Copyright SPRINGER BASEL AG |
Palavras-Chave | #Ischemia and reperfusion injury #INOS #COX-2 #IL-1 beta #Inflammation #Lung and kidney #OXIDE SYNTHASE ACTIVITY #TUMOR-NECROSIS-FACTOR #NITRIC-OXIDE #ISCHEMIA/REPERFUSION INJURY #INTESTINAL ISCHEMIA/REPERFUSION #ADHESION MOLECULE-1 #INHALED PGE(2) #NEUTROPHIL #FAILURE #ASTHMA #Cell Biology #Immunology |
Tipo |
article original article publishedVersion |