Alterations in the profile of blood neutrophil membrane receptors caused by in vivo adrenocorticotrophic hormone actions

Show simple item record Machado, Isabel Daufenback Santin, Jose Roberto Drewes, Carine Cristiane Gil, Cristiane Damas [UNIFESP] Oliani, Sonia Maria Perretti, Mauro Poliselli Farsky, Sandra Helena 2016-01-24T14:38:03Z 2016-01-24T14:38:03Z 2014-11-01
dc.identifier.citation American Journal of Physiology-endocrinology and Metabolism. Bethesda: Amer Physiological Soc, v. 307, n. 9, p. E754-E763, 2014.
dc.identifier.issn 0193-1849
dc.description.abstract Elevated levels of adrenocorticotrophic hormone (ACTH) mobilize granulocytes from bone marrow into the blood, although these neutrophils are refractory to a full migratory response into inflamed tissues. Here, we investigated the dependence of glucocorticoid receptor activation and glucocorticoid-regulated protein annexin A1 (ANXA1) on ACTH-induced neutrophilia and the phenotype of blood neutrophil after ACTH injection, focusing on adhesion molecule expressions and locomotion properties. ACTH injection (5 mu g ip, 4 h) induced neutrophilia in wild-type (WT) mice and did not alter the elevated numbers of neutrophils in RU-38486 (RU)-pretreated or ANXA1(-/-)mice injected with ACTH. Neutrophils from WT ACTH-treated mice presented higher expression of Ly6G(+) ANXA1(high), CD18(high), CD62L(high), CD49(high), CXCR4(high), and formyl-peptide receptor 1 (FPR1(low)) than those observed in RU-pretreated or ANXA1(-/-)mice. the membrane phenotype of neutrophils collected from WT ACTH-treated mice was paralleled by elevated fractions of rolling and adherent leukocytes to the cremaster postcapillary venules together with impaired neutrophil migration into inflamed air pouches in vivo and in vitro reduced formyl-methionyl-leucyl-phenylalanine (fMLP) or stromal-derived factor-1 (SDF-1 alpha)-induced chemotaxis. in an 18-h senescence protocol, neutrophils from WT ACTH-treated mice had a higher proportion of ANXAV(low)/CXCR4(low), and they were less phagocytosed by peritoneal macrophages. We conclude that alterations on HPA axis affect the pattern of membrane receptors in circulating neutrophils, which may lead to different neutrophil phenotypes in the blood. Moreover, ACTH actions render circulating neutrophils to a phenotype with early reactivity, such as in vivo leukocyte-endothelial interactions, but with impaired locomotion and clearance. en
dc.description.sponsorship Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)
dc.description.sponsorship Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)
dc.format.extent E754-E763
dc.language.iso eng
dc.publisher Amer Physiological Soc
dc.relation.ispartof American Journal of Physiology-endocrinology and Metabolism
dc.rights Acesso aberto
dc.subject hypothalamic-pituitary-adrenal axis en
dc.subject chemokine (C-X-C motif) receptor 4 en
dc.subject adhesion molecules en
dc.subject chemotaxis en
dc.subject intravital microscopy en
dc.title Alterations in the profile of blood neutrophil membrane receptors caused by in vivo adrenocorticotrophic hormone actions en
dc.type Artigo
dc.contributor.institution Universidade de São Paulo (USP)
dc.contributor.institution Universidade Federal de São Paulo (UNIFESP)
dc.contributor.institution São Paulo State Univ
dc.contributor.institution Queen Mary Univ London
dc.description.affiliation Univ São Paulo, Fac Pharmaceut Sci, Dept Clin & Toxicol Analyses, BR-05508900 São Paulo, Brazil
dc.description.affiliation Universidade Federal de São Paulo, Dept Morphol & Genet, São Paulo, Brazil
dc.description.affiliation São Paulo State Univ, Inst Biociencias Letras & Ciencias Exatas, Dept Biol, Sao Jose Do Rio Preto, Brazil
dc.description.affiliation Queen Mary Univ London, Barts & London Sch Med, William Harvey Res Inst, London, England
dc.description.affiliationUnifesp Universidade Federal de São Paulo, Dept Morphol & Genet, São Paulo, Brazil
dc.description.sponsorshipID FAPESP: 2010/16828-0
dc.description.sponsorshipID : 2010/08402-2
dc.description.sponsorshipID : 2010/17175-0
dc.description.sponsorshipID : 2010/19802-1
dc.identifier.doi 10.1152/ajpendo.00227.2014
dc.description.source Web of Science
dc.identifier.wos WOS:000344989400003


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