title: Modulation of lung allergic response by renal ischemia and reperfusion injury.
abstract: The Th1/Th2 balance represents an important factor in the pathogenesis of renal ischemia-reperfusion injury (IRI). In addition, IRI causes a systemic inflammation that can affect other tissues, such as the lungs. To investigate the ability of renal IRI to modulate pulmonary function in a specific model of allergic inflammation, C57Bl/6 mice were immunized with ovalbumin/albumen on days 0 and 7 and challenged with an ovalbumin (OA) aerosol on days 14 and 21. After 24 h of the second antigen challenge, the animals were subjected to 45 minutes of ischemia. After 24 h of reperfusion, the bronchoalveolar lavage (BAL) fluid, blood and lung tissue were collected for analysis. Serum creatinine levels increased in both allergic and non-immunized animals subjected to IRI. However, BAL analysis showed a reduction in the total cells (46%) and neutrophils (58%) compared with control allergic animals not submitted to IRI. In addition, OA challenge induced the phosphorylation of ERK and Akt and the expression of inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2) in lung homogenates. After renal IRI, the phosphorylation of ERK and expression of COX-2 and iNOS were markedly reduced; however, there was no difference in the phosphorylation of Akt between sham and ischemic OA-challenged animals. Mucus production was also reduced in allergic mice after renal IRI. IL-4, IL-5 and IL-13 were markedly down-regulated in immunized/challenged mice subjected to IRI. These results suggest that renal IRI can modulate lung allergic inflammation, probably by altering the Th1/Th2 balance and, at least in part, by changing cellular signal transduction factors.
authors.affiliation: Departamento de Imunologia, Instituto de Ciências Biomédicas, Universidade de São Paulo, São Paulo, SP, Brazil.
authors.forename: Gabriela
authors.initials: G
authors.lastname: Campanholle
authors.forename: Reinaldo C
authors.initials: RC
authors.lastname: Silva
authors.forename: Joilson O
authors.initials: JO
authors.lastname: Martins
authors.forename: Maristella A
authors.initials: MA
authors.lastname: Landgraf
authors.forename: Vanessa N
authors.initials: VN
authors.lastname: Paiva
authors.forename: Renaide R
authors.initials: RR
authors.lastname: Ferreira
authors.forename: Mariane T
authors.initials: MT
authors.lastname: Amano
authors.forename: Meire I
authors.initials: MI
authors.lastname: Hiyane
authors.forename: Marcos A
authors.initials: MA
authors.lastname: Cenedeze
authors.forename: Alvaro
authors.initials: A
authors.lastname: Pacheco-Silva
authors.forename: Niels O S
authors.initials: NO
authors.lastname: Camara
authors.forename: Richardt G
authors.initials: RG
authors.lastname: Landgraf
mesh_terms: D000818:Animals; D001772:Blood Cell Count; D001992:Bronchoalveolar Lavage Fluid / Q000276:immunology; D003404:Creatinine / Q000097:blood; D051546:Cyclooxygenase 2 / Q000378:metabolism; D006967:Hypersensitivity / Q000276:immunology / Q000378:metabolism / Q000473:pathology; D007249:Inflammation / Q000276:immunology / Q000378:metabolism / Q000473:pathology; D007378:Interleukins / Q000276:immunology / Q000378:metabolism; D007668:Kidney / Q000276:immunology / Q000293:injuries* / Q000473:pathology; D008168:Lung / Q000276:immunology* / Q000378:metabolism / Q000473:pathology; D020935:MAP Kinase Signaling System; D008297:Male; D051379:Mice; D008810:Mice, Inbred C57BL; D009093:Mucus / Q000276:immunology; D009504:Neutrophils / Q000378:metabolism; D052247:Nitric Oxide Synthase Type II / Q000378:metabolism; D010047:Ovalbumin / Q000008:administration & dosage / Q000276:immunology; D010766:Phosphorylation; D015427:Reperfusion Injury / Q000276:immunology*; D058408:Th1-Th2 Balance
chemical_list: D007378:Interleukins; D010047:Ovalbumin; D003404:Creatinine; D052247:Nitric Oxide Synthase Type II; C496317:Nos2 protein, mouse; C077623:Ptgs2 protein, mouse; D051546:Cyclooxygenase 2