Chlamydia pneumoniae and atherosclerotic disease [Abstract in English]
Autor(a) principal: | |
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Data de Publicação: | 2010 |
Outros Autores: | |
Tipo de documento: | Artigo |
Idioma: | por eng |
Título da fonte: | Scientia Medica (Porto Alegre. Online) |
Texto Completo: | https://revistaseletronicas.pucrs.br/scientiamedica/article/view/5830 |
Resumo: | AIMS: To study the etiopathogenic role of Chlamydia pneumoniae infection in the atherosclerotic disease, in vitro studies and animal models involving Chlamydia pneumonia and atheromatosis were reviewed, as well as clinical assays that analyzed the association between the pathogen and atherosclerotic disease. SOURCE OF DATA: Articles found in Pubmed, SciELO and LILACS data bases, published between 1986 and 2009, were reviewed. SUMMARY OF FINDINGS: Chlamydia pneumoniae can replicate in the endothelium, smooth muscle cells and macrophages, contributing to atherogenesis. Lipopolysacharides and heat-shock proteins originated from the pathogen can induce the formation of foam cells. In vitro, human macrophages infected by Chlamydia pneumoniae induce intracellular accumulation of lipids through a deregulation in the absorption of low-density lipoproteins. In animal models, the pathogen is found in atheroma of hyperlipemic animals, and murine macrophages adhere better to the endothelium when infected by Chlamydia pneumoniae. The sero-epidemiological studies are controversial in terms of the anti-Chlamydia pneumoniae antibody frequency in patients with atherosclerosis. In clinical studies, there is no unequivocal evidence of the benefit of antibiotics on the prognosis of the coronary arterial disease. The occurrence of the infection by Chlamydia pneumonia is not, up to date, a defined risk factor for atherosclerotic disease. CONCLUSIONS: Infection by Chlamydia pneumonia may constitute an important etiopathogenic finding in atheromatosis. However, the clinical relevance of this association, as shown in the epidemiologic and clinical studies herein reviewed , is yet uncertain. |
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Chlamydia pneumoniae and atherosclerotic disease [Abstract in English]Chlamydia pneumoniae e doença ateroscleróticaCHLAMYDOPHILA PNEUMONIAEINFLAMMATIONATHEROSCLEROSISMODELSANIMALIN VITRO.CHLAMYDOPHILA PNEUMONIAEINFLAMAÇÃOATEROSCLEROSEMODELOS ANIMAISIN VITRO.AIMS: To study the etiopathogenic role of Chlamydia pneumoniae infection in the atherosclerotic disease, in vitro studies and animal models involving Chlamydia pneumonia and atheromatosis were reviewed, as well as clinical assays that analyzed the association between the pathogen and atherosclerotic disease. SOURCE OF DATA: Articles found in Pubmed, SciELO and LILACS data bases, published between 1986 and 2009, were reviewed. SUMMARY OF FINDINGS: Chlamydia pneumoniae can replicate in the endothelium, smooth muscle cells and macrophages, contributing to atherogenesis. Lipopolysacharides and heat-shock proteins originated from the pathogen can induce the formation of foam cells. In vitro, human macrophages infected by Chlamydia pneumoniae induce intracellular accumulation of lipids through a deregulation in the absorption of low-density lipoproteins. In animal models, the pathogen is found in atheroma of hyperlipemic animals, and murine macrophages adhere better to the endothelium when infected by Chlamydia pneumoniae. The sero-epidemiological studies are controversial in terms of the anti-Chlamydia pneumoniae antibody frequency in patients with atherosclerosis. In clinical studies, there is no unequivocal evidence of the benefit of antibiotics on the prognosis of the coronary arterial disease. The occurrence of the infection by Chlamydia pneumonia is not, up to date, a defined risk factor for atherosclerotic disease. CONCLUSIONS: Infection by Chlamydia pneumonia may constitute an important etiopathogenic finding in atheromatosis. However, the clinical relevance of this association, as shown in the epidemiologic and clinical studies herein reviewed , is yet uncertain.OBJETIVO: revisar os aspectos etiopatogênicos da infecção por Chlamydia pneumoniae na doença aterosclerótica, analisando estudos em modelos animais e in vitro, assim como ensaios clínicos que avaliaram associação entre a presença do patógeno e doença aterosclerótica. FONTE DE DADOS: foram revisados artigos disponíveis nas bases de dados PubMed, SciELO e LILACS, publicados entre 1986 e 2009. SÍNTESE DOS DADOS: a Chlamydia pneumoniae pode se replicar no endotélio, células musculares lisas e macrófagos, contribuindo para a aterogênese. Lipopolissacarídeos e proteínas de choque térmico oriundos do patógeno podem induzir à formação de células espumosas. In vitro, macrófagos humanos infectados por Chlamydia pneumoniae apresentam acúmulo intracelular de lipídios por desregulação na absorção de lipoproteínas de baixa densidade. Em modelos animais, o patógeno é encontrado no ateroma de animais hiperlipêmicos, e macrófagos murinos aderem melhor ao endotélio quando infectados por Chlamydia pneumoniae. Os estudos soroepidemiológicos são controversos em termos da frequência de anticorpos anti-Chlamydia pneumoniae em pacientes com aterosclerose. Em ensaios clínicos, não há evidência cabal de benefício da terapia antibiótica sobre o prognóstico da doença arterial coronária. A ocorrência de infecção por Chlamydia pneumoniae não é, até o momento, fator de risco definido para doença aterosclerótica. CONCLUSÕES: a infecção por Chlamydia pneumoniae pode constituir achado de importância etiopatogênica na ateromatose. Entretanto, a relevância clínica dessa associação, como mostram os estudos epidemiológicos e ensaios clínicos aqui revisados, ainda é incerta.Editora da PUCRS - ediPUCRS2010-10-19info:eu-repo/semantics/articleinfo:eu-repo/semantics/publishedVersionapplication/pdfapplication/pdfhttps://revistaseletronicas.pucrs.br/scientiamedica/article/view/5830Scientia Medica; Vol. 20 No. 3 (2010); 250-256Scientia Medica; v. 20 n. 3 (2010); 250-2561980-61081806-5562reponame:Scientia Medica (Porto Alegre. Online)instname:Pontifícia Universidade Católica do Rio Grande do Sul (PUCRS)instacron:PUC_RSporenghttps://revistaseletronicas.pucrs.br/scientiamedica/article/view/5830/5482https://revistaseletronicas.pucrs.br/scientiamedica/article/view/5830/5483Sehnem, LucieleStaub, Henrique Luizinfo:eu-repo/semantics/openAccess2013-07-16T12:16:49Zoai:ojs.revistaseletronicas.pucrs.br:article/5830Revistahttps://revistaseletronicas.pucrs.br/scientiamedica/PUBhttps://revistaseletronicas.pucrs.br/scientiamedica/oaiscientiamedica@pucrs.br || editora.periodicos@pucrs.br1980-61081806-5562opendoar:2013-07-16T12:16:49Scientia Medica (Porto Alegre. Online) - Pontifícia Universidade Católica do Rio Grande do Sul (PUCRS)false |
dc.title.none.fl_str_mv |
Chlamydia pneumoniae and atherosclerotic disease [Abstract in English] Chlamydia pneumoniae e doença aterosclerótica |
title |
Chlamydia pneumoniae and atherosclerotic disease [Abstract in English] |
spellingShingle |
Chlamydia pneumoniae and atherosclerotic disease [Abstract in English] Sehnem, Luciele CHLAMYDOPHILA PNEUMONIAE INFLAMMATION ATHEROSCLEROSIS MODELS ANIMAL IN VITRO. CHLAMYDOPHILA PNEUMONIAE INFLAMAÇÃO ATEROSCLEROSE MODELOS ANIMAIS IN VITRO. |
title_short |
Chlamydia pneumoniae and atherosclerotic disease [Abstract in English] |
title_full |
Chlamydia pneumoniae and atherosclerotic disease [Abstract in English] |
title_fullStr |
Chlamydia pneumoniae and atherosclerotic disease [Abstract in English] |
title_full_unstemmed |
Chlamydia pneumoniae and atherosclerotic disease [Abstract in English] |
title_sort |
Chlamydia pneumoniae and atherosclerotic disease [Abstract in English] |
author |
Sehnem, Luciele |
author_facet |
Sehnem, Luciele Staub, Henrique Luiz |
author_role |
author |
author2 |
Staub, Henrique Luiz |
author2_role |
author |
dc.contributor.author.fl_str_mv |
Sehnem, Luciele Staub, Henrique Luiz |
dc.subject.por.fl_str_mv |
CHLAMYDOPHILA PNEUMONIAE INFLAMMATION ATHEROSCLEROSIS MODELS ANIMAL IN VITRO. CHLAMYDOPHILA PNEUMONIAE INFLAMAÇÃO ATEROSCLEROSE MODELOS ANIMAIS IN VITRO. |
topic |
CHLAMYDOPHILA PNEUMONIAE INFLAMMATION ATHEROSCLEROSIS MODELS ANIMAL IN VITRO. CHLAMYDOPHILA PNEUMONIAE INFLAMAÇÃO ATEROSCLEROSE MODELOS ANIMAIS IN VITRO. |
description |
AIMS: To study the etiopathogenic role of Chlamydia pneumoniae infection in the atherosclerotic disease, in vitro studies and animal models involving Chlamydia pneumonia and atheromatosis were reviewed, as well as clinical assays that analyzed the association between the pathogen and atherosclerotic disease. SOURCE OF DATA: Articles found in Pubmed, SciELO and LILACS data bases, published between 1986 and 2009, were reviewed. SUMMARY OF FINDINGS: Chlamydia pneumoniae can replicate in the endothelium, smooth muscle cells and macrophages, contributing to atherogenesis. Lipopolysacharides and heat-shock proteins originated from the pathogen can induce the formation of foam cells. In vitro, human macrophages infected by Chlamydia pneumoniae induce intracellular accumulation of lipids through a deregulation in the absorption of low-density lipoproteins. In animal models, the pathogen is found in atheroma of hyperlipemic animals, and murine macrophages adhere better to the endothelium when infected by Chlamydia pneumoniae. The sero-epidemiological studies are controversial in terms of the anti-Chlamydia pneumoniae antibody frequency in patients with atherosclerosis. In clinical studies, there is no unequivocal evidence of the benefit of antibiotics on the prognosis of the coronary arterial disease. The occurrence of the infection by Chlamydia pneumonia is not, up to date, a defined risk factor for atherosclerotic disease. CONCLUSIONS: Infection by Chlamydia pneumonia may constitute an important etiopathogenic finding in atheromatosis. However, the clinical relevance of this association, as shown in the epidemiologic and clinical studies herein reviewed , is yet uncertain. |
publishDate |
2010 |
dc.date.none.fl_str_mv |
2010-10-19 |
dc.type.driver.fl_str_mv |
info:eu-repo/semantics/article info:eu-repo/semantics/publishedVersion |
format |
article |
status_str |
publishedVersion |
dc.identifier.uri.fl_str_mv |
https://revistaseletronicas.pucrs.br/scientiamedica/article/view/5830 |
url |
https://revistaseletronicas.pucrs.br/scientiamedica/article/view/5830 |
dc.language.iso.fl_str_mv |
por eng |
language |
por eng |
dc.relation.none.fl_str_mv |
https://revistaseletronicas.pucrs.br/scientiamedica/article/view/5830/5482 https://revistaseletronicas.pucrs.br/scientiamedica/article/view/5830/5483 |
dc.rights.driver.fl_str_mv |
info:eu-repo/semantics/openAccess |
eu_rights_str_mv |
openAccess |
dc.format.none.fl_str_mv |
application/pdf application/pdf |
dc.publisher.none.fl_str_mv |
Editora da PUCRS - ediPUCRS |
publisher.none.fl_str_mv |
Editora da PUCRS - ediPUCRS |
dc.source.none.fl_str_mv |
Scientia Medica; Vol. 20 No. 3 (2010); 250-256 Scientia Medica; v. 20 n. 3 (2010); 250-256 1980-6108 1806-5562 reponame:Scientia Medica (Porto Alegre. Online) instname:Pontifícia Universidade Católica do Rio Grande do Sul (PUCRS) instacron:PUC_RS |
instname_str |
Pontifícia Universidade Católica do Rio Grande do Sul (PUCRS) |
instacron_str |
PUC_RS |
institution |
PUC_RS |
reponame_str |
Scientia Medica (Porto Alegre. Online) |
collection |
Scientia Medica (Porto Alegre. Online) |
repository.name.fl_str_mv |
Scientia Medica (Porto Alegre. Online) - Pontifícia Universidade Católica do Rio Grande do Sul (PUCRS) |
repository.mail.fl_str_mv |
scientiamedica@pucrs.br || editora.periodicos@pucrs.br |
_version_ |
1809101749003223040 |