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dc.contributor.authorFranca, Eduardo Luzia
dc.contributor.authorBitencourt, Renata Vieira
dc.contributor.authorFujimori, Mahmi
dc.contributor.authorMorais, Tassiane Cristina de
dc.contributor.authorCalderon, Iracema de Mattos Paranhos [UNESP]
dc.contributor.authorHonorio-Franca, Adenilda Cristina [UNESP]
dc.date.accessioned2014-05-20T13:35:33Z
dc.date.available2014-05-20T13:35:33Z
dc.date.issued2011-02-01
dc.identifierhttp://dx.doi.org/10.1016/j.jmii.2011.01.002
dc.identifier.citationJournal of Microbiology Immunology and Infection. Taipei: Elsevier Taiwan, v. 44, n. 1, p. 1-7, 2011.
dc.identifier.issn1684-1182
dc.identifier.urihttp://hdl.handle.net/11449/12247
dc.description.abstractBackground: Several elements in colostrum and human milk, including antibodies and nonspecific factors with bactericidal and antiviral activity, may play an important anti-infectious and protective role. In developing countries, enterotoxigenic Escherichib coil (ETEC) is the main etiological agent of diarrhea in low-socioeconomic level children. In the present work, we studied the functional activity of mononuclear (MN) and polymorphonuclear (PMN) phagocytes of human colostrum against ETEC, as well as the interactions between these cells and colostral or serum opsonins.Methods: Colostrum samples were collected from 33 clinically healthy women between 48 and 72 hours postpartum. We verified superoxide release in colostral MN and PMN using cytochrome C reduction methods, phagocytosis, and bactericidal activity using acridine orange methods and superoxide dismutase (SOD) in the colostrum supernatants.Results: Colostral MN and PMN phagocytes exposed to ETEC opsonized with colostrum supernatants caused a significant increase (p < 0.05) in superoxide release. Phagocytosis by colostral PMN cells increased significantly (p < 0.5) when the phagocytes were incubated with both sources of opsonins (sera and colostrum). Increases in superoxide release in the presence of opsonized bacteria triggered the bactericidal activity of the phagocytes. Phagocyte treatment with SOD decreased their ability to eliminate ETEC. Colostrum supernatant had higher SOD concentrations (p < 0.05) compared with normal human sera.Conclusions: These results suggest that the ability of phagocytes to eliminate ETEC depends on the activation of cellular oxidative metabolism; moreover, activation of colostral phagocytes is likely an additional breast-feeding protection mechanism against intestinal infections in infants. Copyright (C) 2011, Taiwan Society of Microbiology. Published by Elsevier Taiwan LLC. All rights reserved.en
dc.description.sponsorshipFundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)
dc.description.sponsorshipFundação de Amparo à Pesquisa do Estado de Mato Grosso (FAPEMAT)
dc.language.isoeng
dc.publisherElsevier Taiwan
dc.relation.ispartofJournal of Microbiology, Immunology and Infection
dc.sourceWeb of Science
dc.subjectColostrumen
dc.subjectEnterotoxigenicen
dc.subjectEscherichia coilen
dc.subjectMicrobicidal activityen
dc.subjectPhagocyteen
dc.titleHuman colostral phagocytes eliminate enterotoxigenic Escherichia coli opsonized by colostrum supernatanten
dc.typeArtigo
dcterms.licensehttp://www.elsevier.com/about/open-access/open-access-policies/article-posting-policy
dcterms.rightsHolderElsevier Taiwan
dc.contributor.institutionUniv Fed Mato Grosso
dc.contributor.institutionUniv Ctr Planalto Araxa
dc.contributor.institutionUniversidade Estadual Paulista (UNESP)
dc.description.affiliationUniv Fed Mato Grosso, Inst Biol Sci & Hlth, BR-78698000 Pontal do Araguaia, Mato Grosso, Brazil
dc.description.affiliationUniv Ctr Planalto Araxa, Inst Hlth Sci, Araxa, Minas Gerais, Brazil
dc.description.affiliationSão Paulo State Univ, Botucatu Med Sch, Postgrad Program Gynecol Obstet & Mastol, São Paulo, Brazil
dc.description.affiliationUnespSão Paulo State Univ, Botucatu Med Sch, Postgrad Program Gynecol Obstet & Mastol, São Paulo, Brazil
dc.identifier.doi10.1016/j.jmii.2011.01.002
dc.identifier.wosWOS:000288627600001
dc.rights.accessRightsAcesso restrito
dc.description.sponsorshipIdFAPESP: 08/09187-8
dc.description.sponsorshipIdFAPEMAT: 735593/2008
dc.description.sponsorshipIdFAPEMAT: 453387/2009
unesp.campusUniversidade Estadual Paulista (UNESP), Faculdade de Medicina, Botucatupt
dc.identifier.lattes0679387622604743
unesp.author.lattes0679387622604743
unesp.author.orcid0000-0003-4761-4336[5]
dc.relation.ispartofjcr2.094
dc.relation.ispartofsjr0,789
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