Airway exposure to staphylococcal enterotoxin A potentiates allergen-induced bone marrow eosinophilia and trafficking to peripheral blood and airways

dc.creatorSquebola-Cola, DM
dc.creatorMello, GC
dc.creatorPissinatti, L
dc.creatorSchenka, AA
dc.creatorAnhe, GF
dc.creatorDeSouza, IA
dc.creatorCondino-Neto, A
dc.creatorAntunes, E
dc.date2013
dc.dateMAY
dc.date2014-08-01T18:19:10Z
dc.date2015-11-26T17:04:16Z
dc.date2014-08-01T18:19:10Z
dc.date2015-11-26T17:04:16Z
dc.date.accessioned2018-03-28T23:52:32Z
dc.date.available2018-03-28T23:52:32Z
dc.identifierAmerican Journal Of Physiology-lung Cellular And Molecular Physiology. Amer Physiological Soc, v. 304, n. 10, n. L639, n. L645, 2013.
dc.identifier1040-0605
dc.identifierWOS:000318966800001
dc.identifier10.1152/ajplung.00025.2013
dc.identifierhttp://www.repositorio.unicamp.br/jspui/handle/REPOSIP/77106
dc.identifierhttp://repositorio.unicamp.br/jspui/handle/REPOSIP/77106
dc.identifier.urihttp://repositorioslatinoamericanos.uchile.cl/handle/2250/1279301
dc.descriptionBone marrow (BM) eosinopoiesis is a common feature during allergen exposure in atopic individuals. Airway exposure to staphylococcal superantigens aggravates allergic airway disease and increases the output of BM eosinophils. However, the exact mechanisms regulating eosinophil mobilization and trafficking to the peripheral circulation and airways remain to be elucidated. Therefore, this study aimed to investigate the mechanisms determining the BM eosinopoiesis in allergic mice under exposure to staphylococcal enterotoxin A (SEA). Ovalbumin (OVA)-sensitized male BALB/C mice were intranasally exposed to SEA (1 mu g), and at 4, 12, 24, and 48 h later animals were challenged with OVA (10 mu g, twice a day). Measurement of IL-5, eotaxin, and granulocyte-macrophage colony-stimulating factor (GMCSF) levels, flow cytometry for CCR3(+), VLA4(+), and CCR3(+)VLA4(+), as well as adhesion assays to VCAM-1 were performed in BM. Prior airway exposure to SEA time dependently increased the BM eosinophil number in OVA-challenged mice. Eosinophils gradually disappear from peripheral blood, being recruited over time to the airways, where they achieve a maximal infiltration at 24 h. SEA exposure increased the levels of IL-5 and eotaxin (but not GM-CSF) in BM of OVA-challenged mice. Marked increases in CCR3(+) and CCR3(+)VLA4(+) expressions in BM eosinophils of OVA-challenged mice were observed, an effect largely reduced by prior exposure to SEA. Adhesion of BM eosinophils to VCAM-1 was increased in OVA-challenged mice, but prior SEA exposure abrogated this enhanced cell adhesion. Accumulation of BM eosinophils by airway SEA exposure takes place through IL-5- and CCR3-dependent mechanisms, along with downregulation of CCR3/VL4 and impaired cell adhesion to VCAM-1.
dc.description304
dc.description10
dc.descriptionL639
dc.descriptionL645
dc.languageen
dc.publisherAmer Physiological Soc
dc.publisherBethesda
dc.publisherEUA
dc.relationAmerican Journal Of Physiology-lung Cellular And Molecular Physiology
dc.relationAm. J. Physiol.-Lung Cell. Mol. Physiol.
dc.rightsfechado
dc.sourceWeb of Science
dc.subjectovalbumin
dc.subjecteotaxin
dc.subjectIL-5
dc.subjectCCR3
dc.subjectVLA4
dc.subjectVCAM-1
dc.subjectasthma
dc.subjectSevere Atopic-dermatitis
dc.subjectCd34(+) Cells
dc.subjectMicrobial Superantigens
dc.subjectBacterial Superantigen
dc.subjectPulmonary Inflammation
dc.subjectCommitted Progenitors
dc.subjectAsthmatic Subjects
dc.subjectDependent Airway
dc.subjectMurine Model
dc.subjectIn-vivo
dc.titleAirway exposure to staphylococcal enterotoxin A potentiates allergen-induced bone marrow eosinophilia and trafficking to peripheral blood and airways
dc.typeArtículos de revistas


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