Show simple item record

dc.rights.licensehttp://creativecommons.org/licenses/by-nc-sa/3.0/ve/
dc.contributor.authorVielma, Silvanaes_VE
dc.contributor.authorVirella, Gabrieles_VE
dc.contributor.authorGorod, Adam J.es_VE
dc.contributor.authorLopes Virella, Maria F.es_VE
dc.date2006-02-24es_VE
dc.date.accessioned2006-02-24T09:00:00Z
dc.date.available2006-02-24T09:00:00Z
dc.date.created2002-01-01es_VE
dc.date.issued2006-02-24T09:00:00Zes_VE
dc.identifier.otherT016300002211/0es_VE
dc.identifier.urihttp://www.saber.ula.ve/handle/123456789/16109
dc.description.abstractChlamydophila pneumoniae infection of human aortic endothelial cells induces the expression of fc y receptor II (FCyRII). (Vielma, Silvana; Virella, Gabriel; Gorod, Adam J.; Lopes Virella, Maria F.) Abstract Chronic endothelial infection is believed to be one of the factors able to cause endothelial cell damage and trigger the onset of human atherosclerosis. Chlamydophila pneumoniae infects endothelial cells and has received special attention because of both epidemiological and experimental evidence supporting its role as a risk factor for atherosclerosis. It is also possible that otherwise independent risk factors for atherosclerosis may have synergistic effects. Immune phenomena, such as the formation of circulating immune complexes (IC) containing modified LDL and corresponding antibodies, have been linked to the development of coronary artery disease. The antibodies involved in the immune response to modified lipoproteins are predominantly of the pro-inflammatory IgG1 and IgG3 subclasses. However, it is difficult to understand how circulating IC could cause endothelial damage and initiate the atherosclerotic process, unless they were formed in the subendothelial space or immobilized by endothelial cells. The last hypothesis would be possible if endothelial cells expressed Fcy receptors. Healthy endothelial cells do not express Fcy receptors, but endothelial cells infected by a variety of infectious agents do. Thus we decided to investigate whether infection of endothelial cells with C. pneumoniae is also able to cause the expression of Fcy receptors. The expression of Fcy receptors (CD64, 32, and 16) on human aortic endothelial cells infected with C. pneumoniae for 4, 24, 36, and 48 h was studied by flow cytometry. Twenty-four hours after infection 30-40% of the endothelial cells had detectable inclusion bodies, 8-9% of the total number of cells (approximately 25% of the infected cells) expressed FcyRII, and about 1.5-2% (5% of infected cells) expressed FcyRI and FcyRIII. Double-staining studies confirmed that the expression of FcyRII was limited to C. pneumoniae- infected endothelial cells. We conclude that C. pneumoniae infection induces primarily the expression of FcyRII by endothelial cells and this may be a significant link between two proposed pathogenic mechanisms involved in the pathogenesis of human atherosclerosis. Published on: Clinical Immunology Vol. 104, No. 3, September, pp. 265-273, 2002 doi:10.1006/clim.2002.5237es_VE
dc.language.isoeses_VE
dc.publisherSABER ULAes_VE
dc.rightsinfo:eu-repo/semantics/openAccess
dc.titleChlamydophila pneumoniae infection of human aortic endothelial cells induces the expression of fc y receptor II (FCyRII)es_VE
dc.typeinfo:eu-repo/semantics/article
dc.description.emailvielmasa@musc.edues_VE
dc.description.tiponivelNivel monográficoes_VE
dc.subject.departamentoDepartamento de Microbiología y Parasitologíaes_VE
dc.subject.escuelaEscuela de Medicinaes_VE
dc.subject.facultadFacultad de Medicinaes_VE
dc.subject.keywordsChlamydophila pneumoniaees_VE
dc.subject.keywordsFcy receptorses_VE
dc.subject.keywordsAtherosclerosises_VE
dc.subject.keywordsEndothelial dysfunctiones_VE
dc.subject.laboratorioLaboratorio de Microbiología y Salud Pública del Estado Mérida. ULA-ULEes_VE
dc.subject.tipoArtículoses_VE


Files in this item

Thumbnail
Thumbnail

This item appears in the following Collection(s)

Show simple item record