Macrophage suppression following phagocytosis of apoptotic neutrophils is mediated by the S100A9 calcium-binding protein

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dc.contributor.authorDe Lorenzo, B. H. P.
dc.contributor.authorGodoy, L. C.
dc.contributor.authorNovaes e Brito, R. R.
dc.contributor.authorPagano, R. L.
dc.contributor.authorAmorim-Dias, M. A.
dc.contributor.authorGrosso, D. M.
dc.contributor.authorLopes, J. D.
dc.contributor.authorMariano, M. [UNESP]
dc.contributor.institutionUniversidade Federal de São Paulo (UNIFESP)
dc.contributor.institutionMIT
dc.contributor.institutionUniversidade de São Paulo (USP)
dc.contributor.institutionHosp Alemao Oswaldo Cruz
dc.contributor.institutionUniversidade Estadual Paulista (Unesp)
dc.date.accessioned2014-05-20T15:33:11Z
dc.date.available2014-05-20T15:33:11Z
dc.date.issued2010-05-01
dc.description.abstractThe clearance of apoptotic cells by phagocytes is a fundamental process during tissue remodeling and resolution of inflammation. In turn, the phagocytosis of apoptotic cells generates signals that suppress pro-inflammatory activation of macrophages. These events occur during the resolution phase of inflammation and therefore the malfunctioning of this process may lead to inflammation-related tissue damage. Here, we demonstrate that the calcium-binding protein S100A9, normally abundant in the cytoplasm of neutrophils and also released by apoptotic neutrophils, is involved in the suppression of macrophages after the uptake of apoptotic neutrophils. Both, spontaneous and induced production of inflammatory species (nitric oxide, hydrogen peroxide and TNF-alpha) as well as the phagocytic activity were inhibited when macrophages were in presence of apoptotic neutrophils, conditioned medium from neutrophil cultures or a peptide corresponding to the C-terminal region of S100A9 protein. on the other hand, macrophages kept in the conditioned medium of neutrophils that was previously depleted of S100A9 were shown to resume the activated status. Finally, we demonstrate that the calcium-binding property of S100A9 might play a role in the suppression process, since the stimulation of intracellular calcium release with ionomycin significantly reversed the effects of the uptake of apoptotic neutrophils in macrophages. In conclusion, we propose that S100A9 is a novel component of the regulatory mechanisms of inflammation, acting side-by-side with other suppressor factors generated upon ingestion of apoptotic cells. (C) 2009 Elsevier GmbH. All rights reserved.en
dc.description.affiliationUniv Fed São Paulo, Dept Microbiol Immunol & Parasitol, Discipline Immunol, BR-04023900 São Paulo, Brazil
dc.description.affiliationMIT, Dept Biol Engn, Cambridge, MA 02140 USA
dc.description.affiliationUniv São Paulo, Inst Biomed Sci, Dept Phys & Biophys, BR-05508900 São Paulo, Brazil
dc.description.affiliationHosp Alemao Oswaldo Cruz, Ludwig Inst Canc Res, BR-01323903 São Paulo, Brazil
dc.description.affiliationUniv Estadual Paulista, Discipline Immunol, BR-04026002 São Paulo, Brazil
dc.description.affiliationUnespUniv Estadual Paulista, Discipline Immunol, BR-04026002 São Paulo, Brazil
dc.description.sponsorshipCoordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES)
dc.description.sponsorshipFundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)
dc.format.extent341-347
dc.identifierhttp://dx.doi.org/10.1016/j.imbio.2009.05.013
dc.identifier.citationImmunobiology. Jena: Elsevier Gmbh, Urban & Fischer Verlag, v. 215, n. 5, p. 341-347, 2010.
dc.identifier.doi10.1016/j.imbio.2009.05.013
dc.identifier.issn0171-2985
dc.identifier.urihttp://hdl.handle.net/11449/41893
dc.identifier.wosWOS:000277829800001
dc.language.isoeng
dc.publisherElsevier Gmbh, Urban & Fischer Verlag
dc.relation.ispartofImmunobiology
dc.relation.ispartofjcr2.873
dc.relation.ispartofsjr1,100
dc.rights.accessRightsAcesso restrito
dc.sourceWeb of Science
dc.subjectApoptotic neutrophilsen
dc.subjectCalcium-binding proteinsen
dc.subjectInflammationen
dc.subjectMacrophage suppressionen
dc.subjectResistance to infectionen
dc.subjectS100A9en
dc.titleMacrophage suppression following phagocytosis of apoptotic neutrophils is mediated by the S100A9 calcium-binding proteinen
dc.typeArtigo
dcterms.licensehttp://www.elsevier.com/about/open-access/open-access-policies/article-posting-policy
dcterms.rightsHolderElsevier Gmbh, Urban & Fischer Verlag

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