Staphylococcal Enterotoxin A Regulates Bone Marrow Granulocyte Trafficking During Pulmonary Inflammatory Disease In Mice

dc.creatorTakeshita
dc.creatorW. M.; Gushiken
dc.creatorV. O.; Ferreira-Duarte
dc.creatorA. P.; Pinheiro-Torres
dc.creatorA. S.; Roncalho-Buck
dc.creatorI. A.; Squebola-Cola
dc.creatorD. M.; Mello
dc.creatorG. C.; Anhe
dc.creatorG. F.; Antunes
dc.creatorE.; DeSouza
dc.creatorI. A.
dc.date2015-SEP
dc.date2016-06-07T13:21:22Z
dc.date2016-06-07T13:21:22Z
dc.date.accessioned2018-03-29T01:41:14Z
dc.date.available2018-03-29T01:41:14Z
dc.identifier
dc.identifierStaphylococcal Enterotoxin A Regulates Bone Marrow Granulocyte Trafficking During Pulmonary Inflammatory Disease In Mice. Academic Press Inc Elsevier Science, v. 287, p. 267-275 SEP-2015.
dc.identifier0041-008X
dc.identifierWOS:000360422800010
dc.identifier10.1016/j.taap.2015.06.013
dc.identifierhttp://www.sciencedirect.com/science/article/pii/S0041008X1530020X
dc.identifierhttp://repositorio.unicamp.br/jspui/handle/REPOSIP/243070
dc.identifier.urihttp://repositorioslatinoamericanos.uchile.cl/handle/2250/1306768
dc.descriptionFundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)
dc.descriptionPulmonary 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.
dc.description287
dc.description3
dc.description
dc.description267
dc.description275
dc.descriptionFundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)
dc.descriptionFundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)
dc.descriptionFAPESP [2009/16522-0]
dc.description
dc.description
dc.description
dc.languageen
dc.publisherACADEMIC PRESS INC ELSEVIER SCIENCE
dc.publisher
dc.publisherSAN DIEGO
dc.relationTOXICOLOGY AND APPLIED PHARMACOLOGY
dc.rightsembargo
dc.sourceWOS
dc.subjectNeutrophil Mobilization
dc.subjectAirway Exposure
dc.subjectBacterial Superantigen
dc.subjectAureus Pneumonia
dc.subjectDependent Airway
dc.subjectLung Injury
dc.subjectTnf-alpha
dc.subjectG-csf
dc.subjectChemokines
dc.subjectHematopoiesis
dc.titleStaphylococcal Enterotoxin A Regulates Bone Marrow Granulocyte Trafficking During Pulmonary Inflammatory Disease In Mice
dc.typeArtículos de revistas


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