Catalogo Articoli (Spogli Riviste)

OPAC HELP

Titolo:
Chlamydia pneumoniae-infected monocytes exhibit increased adherence to human aortic endothelial cells
Autore:
Kalayoglu, MV; Perkins, BN; Byrne, GI;
Indirizzi:
Univ Wisconsin, Sch Med, Dept Med Microbiol & Immunol, Madison, WI 53706 USA Univ Wisconsin Madison WI USA 53706 biol & Immunol, Madison, WI 53706 USA
Titolo Testata:
MICROBES AND INFECTION
fascicolo: 12, volume: 3, anno: 2001,
pagine: 963 - 969
SICI:
1286-4579(200110)3:12<963:CPMEIA>2.0.ZU;2-U
Fonte:
ISI
Lingua:
ENG
Soggetto:
LOW-LEVEL HYPERCHOLESTEROLEMIA; FATTY STREAK CONVERSION; LOW-DENSITY-LIPOPROTEIN; NONHUMAN PRIMATE; SHEAR-STRESS; VASCULAR ENDOTHELIUM; CIGARETTE-SMOKING; CYTOKINE RESPONSE; FIBROUS PLAQUE; IN-VITRO;
Keywords:
Chlamydia pneumoniae; atherosclerosis; monocytes; endothelial cells, human;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
57
Recensione:
Indirizzi per estratti:
Indirizzo: Kalayoglu, MV Univ Wisconsin, Sch Med, Dept Med Microbiol & Immunol, 436 SMI,1300 Univ Ave, Madison, WI 53706 USA Univ Wisconsin 436 SMI,1300 Univ Ave Madison WI USA 53706 SA
Citazione:
M.V. Kalayoglu et al., "Chlamydia pneumoniae-infected monocytes exhibit increased adherence to human aortic endothelial cells", MICROBES IN, 3(12), 2001, pp. 963-969

Abstract

Interactions between monocytes and endothelial cells play an important role in the pathogenesis of atherosclerosis, and monocyte adhesion to arterialendothelium is one of the earliest events in atherogenesis. Work presentedin this study examined human monocyte adherence to primary human aortic endothelial cells following monocyte infection with Chlamydia pneumoniae, an intracellular pathogen associated with atherosclerosis by a variety of sero-epidemiological, pathological and functional studies. Infected monocytes exhibited enhanced adhesion to aortic endothelial cells in a time- and dose-dependent manner. Pre-treatment of C. pneumoniae with heat did not effect the organism's capacity to enhance monocyte adhesion, suggesting that heat-stable chlamydial antigens such as chlamydial lipopolysaccharide (cLPS) mediated monocyte adherence. Indeed, treatment of monocytes with cLPS was sufficient to increase monocyte adherence to endothelial cells, and increased adherence of infected or cLPS-treated monocytes could be inhibited by the LPSantagonist lipid X. Moreover, C, pneumoniae-induced adherence could be inhibited by incubating monocytes with a mAb specific to the human beta2-integrin chain, suggesting that enhanced adherence resulted from increased expression of these adhesion molecules. These data show that C. pneumoniae can enhance the capacity of monocytes to adhere to primary human aortic endothelial cells. The enhanced adherence exhibited by infected monocytes may increase monocyte residence time in vascular sites with reduced wall shear stress and promote entry of infected cells into lesion-prone locations. (C) 2001Editions scientifiques et medicales Elsevier SAS.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 29/03/20 alle ore 12:01:17