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Type: Artigo de periódico
Title: Inflammatory Mechanisms Underlying The Rat Pulmonary Neutrophil Influx Induced By Airway Exposure To Staphylococcal Enterotoxin Type A.
Author: Desouza, Ivani A
Franco-Penteado, Carla F
Camargo, Enilton A
Lima, Carmen S P
Teixeira, Simone A
Muscará, Marcelo N
De Nucci, Gilberto
Antunes, Edson
Abstract: Association between staphylococcal infection and pathogenesis of upper airways disease has been reported. This study aimed to investigate the mechanisms underlying the rat pulmonary inflammation induced by airway exposure to staphylococcal enterotoxin A (SEA). SEA (0.3-10 ng trachea(-1)) caused dose-dependent neutrophil accumulation in BAL fluid, reaching maximal responses at 4 h (25-fold increase for 3 ng trachea(-1)). Significant accumulation of both lymphocytes and macrophages in BAL fluid was also observed at 4 h (2.1- and 1.9-fold increase, respectively, for 3 ng trachea(-1)). At later times (16 h), neutrophil counts in bone marrow (immature forms) and peripheral blood increased by 63 and 81%, respectively. SEA failed to directly induce chemotaxis and adhesion of isolated neutrophils. Analysis of mRNA expression for iNOS, COX-2 and CINC-2 in lung tissue showed an upregulation of these enzymes, which paralleled elevated levels of LTB4, PGE2, TNF-alpha, IL-6 and NO2- in BAL fluid. Expression of CINC-1 was unchanged, whereas CINC-3 was reduced in SEA-treated rats. Incubation of isolated alveolar macrophages with SEA (3 microg ml(-1)) resulted in significant elevations of TNF-alpha and NO2- levels in the cell supernatants. Dexamethasone (0.5 mg kg(-1)), celecoxib (3 mg kg(-1)) and compound 1400 W (5 mg kg(-1)) markedly reduced SEA-induced lung neutrophil influx and NO2- levels in BAL fluid. The lipoxygenase inhibitor AA-861 (100 microg kg(-1)) partly inhibited the neutrophil influx in SEA-treated rats without modifying the NO2- levels. None of these treatments reduced the number of mononuclear cells in BAL fluid (except of dexamethasone, which abolished the increased lymphocyte counts). Our study shows that airways exposure to SEA results in marked neutrophil influx through mechanisms involving increased expressions of CINC-2, iNOS and COX-2, as well as enhanced production of NO, PGE2, LTB4, TNF-alpha and IL-6.
Subject: Animals
Bronchoalveolar Lavage Fluid
Chemokine Cxcl1
Chemokines, Cxc
Chemotaxis, Leukocyte
Cyclooxygenase 2
Intercellular Signaling Peptides And Proteins
Leukocytes, Mononuclear
Leukotriene B4
Macrophages, Alveolar
N-formylmethionine Leucyl-phenylalanine
Neutrophil Infiltration
Nitric Oxide Synthase Type Ii
Rna, Messenger
Rats, Wistar
Tumor Necrosis Factor-alpha
Citation: British Journal Of Pharmacology. v. 146, n. 6, p. 781-91, 2005-Nov.
Rights: fechado
Identifier DOI: 10.1038/sj.bjp.0706393
Date Issue: 2005
Appears in Collections:Unicamp - Artigos e Outros Documentos

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