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(Reference retrieved automatically from Web of Science through information on FAPESP grant and its corresponding number as mentioned in the publication by the authors.)

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

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Author(s):
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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]
Total Authors: 14
Affiliation:
[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
Total Affiliations: 5
Document type: Journal article
Source: Inflammation Research; v. 59, n. 10, p. 861-869, OCT 2010.
Web of Science Citations: 17
Abstract

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)

FAPESP's process: 07/07139-3 - The role of heme oxygenase 1 in different renal inflammatory process in experimental animal models
Grantee:Niels Olsen Saraiva Câmara
Support Opportunities: Research Projects - Thematic Grants
FAPESP's process: 06/03982-5 - Molecular aspects involved in leukocytes microbicidal and inflammatory activities in the lung
Grantee:Sônia Jancar
Support Opportunities: Research Projects - Thematic Grants