Acute pulmonary inflammation induced by exposure of the airways to staphylococcal enterotoxin type B in rats

Journal Article · Wed Nov 15 00:00:00 EST 2006 · Toxicology and Applied Pharmacology

DOI:https://doi.org/10.1016/j.taap.2006.07.001· OSTI ID:20850483

Desouza, Ivani A ^[1]; Franco-Penteado, Carla F ^[1]; Camargo, Enilton A ^[1]; Lima, Carmen S.P. ^[2]; Teixeira, Simone A ^[3]; Muscara, Marcelo N ^[3]; De Nucci, Gilberto ^[1]; Antunes, Edson ^[1]

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1. Department of Pharmacology, State University of Campinas (UNICAMP), P.O. Box 6111, 13084-971, Campinas (SP) (Brazil)
2. Laboratory of Haemathology of Faculty of Medical Sciences, State University of Campinas (UNICAMP), P.O. Box 6111, 13084-971, Campinas (SP) (Brazil)
3. Department of Pharmacology, Institute of Biomedical Sciences, University of Sao Paulo (USP), Sao Paulo (SP) (Brazil)

Staphylocococcus aureus is a gram-positive bacterium that produces several enterotoxins, which are responsible for most part of pathological conditions associated to staphylococcal infections, including lung inflammation. This study aimed to investigate the underlying inflammatory mechanisms involved in leukocyte recruitment in rats exposed to staphylococcal enterotoxin B (SEB). Rats were anesthetized with pentobarbital sodium and intratracheally injected with either SEB or sterile phosphate-buffered saline (PBS, 0.4 ml). Airways exposition to SEB (7.5-250 ng/trachea) caused a dose- and time-dependent neutrophil accumulation in BAL fluid, the maximal effects of which were observed at 4 h post-SEB exposure (250 ng/trachea). Eosinophils were virtually absent in BAL fluid, whereas mononuclear cell counts increased only at 24 h post-SEB. Significant elevations of granulocytes in bone marrow (mature and immature forms) and peripheral blood have also been detected. In BAL fluid, marked elevations in the levels of lipid mediators (LTB{sub 4} and PGE{sub 2}) and cytokines (TNF-{alpha}, IL-6 and IL-10) were observed after SEB instillation. The SEB-induced neutrophil accumulation in BAL fluid was reduced by pretreatment with dexamethasone (0.5 mg/kg), the COX-2 inhibitor celecoxib (3 mg/kg), the selective iNOS inhibitor compound 1400 W (5 mg/kg) and the lipoxygenase inhibitor AA-861 (200 {mu}g/kg). In separate experiments carried out with rat isolated peripheral neutrophils, SEB failed to induce neutrophil adhesion to serum-coated plates and chemotaxis. In conclusion, rat airways exposition to SEB causes a neutrophil-dependent lung inflammation at 4 h as result of the release of proinflammatory (NO, PGE{sub 2}, LTB{sub 4}, TNF-{alpha}, IL-6) and anti-inflammatory mediators (IL-10)

• OSTI ID: 20850483
• Journal Information: Toxicology and Applied Pharmacology, Vol. 217, Issue 1; Other Information: DOI: 10.1016/j.taap.2006.07.001; PII: S0041-008X(06)00233-X; Copyright (c) 2006 Elsevier Science B.V., Amsterdam, The Netherlands, All rights reserved; Country of input: International Atomic Energy Agency (IAEA); ISSN 0041-008X
• Country of Publication: United States
• Language: English

Related Subjects

60 APPLIED LIFE SCIENCES
ARGININE
BACTERIA
BONE MARROW
CARBON MONOXIDE
DEXAMETHASONE
ELECTROMECHANICS
EOSINOPHILS
ESTERS
INDIUM OXIDES
INFLAMMATION
LAVAGE
LIPIDS
LUNGS
LYMPHOKINES
MICROSTRUCTURE
NECROSIS
NEMBUTAL
NEUTROPHILS
NITRIC OXIDE
OMEGA BARYONS
PHOSPHATES
PROSTAGLANDINS
RATS
TIME DEPENDENCE
TRACHEA