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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.)

Staphylococcal enterotoxin A regulates bone marrow granulocyte trafficking during pulmonary inflammatory disease in mice

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Author(s):
Takeshita, W. M. [1] ; Gushiken, V. O. [1] ; Ferreira-Duarte, A. P. [1] ; Pinheiro-Torres, A. S. [1] ; Roncalho-Buck, I. A. [1] ; Squebola-Cola, D. M. [2] ; Mello, G. C. [2] ; Anhe, G. F. [2] ; Antunes, E. [2] ; DeSouza, I. A. [1]
Total Authors: 10
Affiliation:
[1] Fac Med Jundiai FMJ, Dept Biol & Physiol, BR-13202550 Jundiai, SP - Brazil
[2] Univ Campinas UNICAMP, Fac Med Sci, Dept Pharmacol, Campinas, SP - Brazil
Total Affiliations: 2
Document type: Journal article
Source: Toxicology and Applied Pharmacology; v. 287, n. 3, p. 267-275, SEP 15 2015.
Web of Science Citations: 1
Abstract

Pulmonary neutrophil infiltration produced by Staphylococcal enterotoxin A (SEA) airway exposure is accompanied by marked granulocyte accumulation in bone marrow (BM). Therefore, the aim of this study was to investigate the mechanisms of BM cell accumulation, and trafficking to circulating blood and lung tissue after SEA airway exposure. Male BALB/C mice were intranasally exposed to SEA (1 mu g), and at 4, 12 and 24 h thereafter, BM, circulating blood, bronchoalveolar lavage (BAL) fluid and lung tissue were collected. Adhesion of BM granulocytes and flow cytometry for MAC-1, LFA1-alpha and VLA-4 and cytokine and/or chemokine levels were assayed after SEA-airway exposure. Prior exposure to SEA promoted a marked PMN influx to BAL and lung tissue, which was accompanied by increased counts of immature and/or mature neutrophils and eosinophils in BM, along with blood neutrophilia. Airway exposure to SEA enhanced BM neutrophil MAC-1 expression, and adhesion to VCAM-1 and/or ICAM-1-coated plates. Elevated levels of GM-CSF, G-CSF, KC/CXCL-1 and SDF-1 alpha were detected in BM after SEA exposure. SEA exposure increased production of eosinopoietic cytokines (eotaxin and IL-5) and BM eosinophil VLA-4 expression, but it failed to affect eosinophil adhesion to VCAM-1 and ICAM-1. In conclusion, BM neutrophil accumulation after SEA exposure takes place by integrated action of cytokines and/or chemokines, enhancing the adhesive responses of BM neutrophils and its trafficking to lung tissues, leading to acute lung injury. BM eosinophil accumulation in SEA-induced acute lung injury may occur via increased eosinopoietic cytokines and VIA-4 expression. (C) 2015 Published by Elsevier Inc. (AU)

FAPESP's process: 09/16522-0 - Effects of staphylococcal enterotoxins (SEs) on the mice bone marrow mature granulocytes production and functions
Grantee:Ivani Aparecida de Souza
Support Opportunities: Research Grants - Young Investigators Grants