Neutrophils Endothelium Interaction
Mostrando 1-6 de 6 artigos, teses e dissertações.
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1. Modulation by melatonin of the neutrophils-endothelium interaction in vitro: action on endothelial cells / Modulação da interação neutrófilo-endotélio in vitro por melatonina: ação sobre as células endoteliais
Melatonina, indolamina amplamente distribuída entre os seres vivos, é o hormônio da glândula pineal e também é produzida de forma parácrina por células imunocompetentes estimuladas. A produção de melatonina pela glândula pineal ocorre apenas no escuro e este hormônio serve para marcar a existência e a duração da noite. A monocamada de células
IBICT - Instituto Brasileiro de Informação em Ciência e Tecnologia. Publicado em: 07/11/2011
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2. Neutrophil-endothelial cell interactions. Modulation of neutrophil adhesiveness induced by complement fragments C5a and C5a des arg and formyl-methionyl-leucyl-phenylalanine in vitro.
Neutrophil adherence to vascular endothelial cells is the initial event in the emigration of neutrophils through blood vessel walls to tissue sites of inflammation; this process is attributed to the generation of extravascular chemotactic factors. To investigate the effect of chemotactic factors on neutrophil adherence to endothelium, we developed a sensitiv
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3. Adherence of neutrophils to cultured human microvascular endothelial cells. Stimulation by chemotactic peptides and lipid mediators and dependence upon the Mac-1, LFA-1, p150,95 glycoprotein family.
The process of neutrophil adhesion to and migration through the microvascular endothelium, an early event in the induction of the acute inflammatory response, has been attributed to the generation of extravascular chemoattractants. Although both chemotactic peptides and lipid mediators enhance neutrophil adherence in vitro and in vivo, the mechanism(s) invol
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4. Prevention of in vitro neutrophil-endothelial attachment through shedding of L-selectin by nonsteroidal antiinflammatory drugs.
The activation of the endothelial cells by extravascular stimuli is the key event in the extravasation of circulating leukocytes to target tissues. L-selectin, a member of the selectin family, is constitutively expressed by white cells, and is the molecule involved in the initial binding of leukocytes to activated endothelium. After activation, leukocytes ra
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5. Prevention of In vitro neutrophil adhesion to endothelial cells through shedding of L-selectin by C-reactive protein and peptides derived from C-reactive protein.
C-Reactive protein (CRP), the classic acute-phase reactant in humans, diminishes accumulation of neutrophils at inflammatory sites. To evaluate the underlying mechanisms, we have studied whether CRP and peptides derived from CRP could affect the first step of neutrophil extravasation, the L-selectin-mediated interaction of neutrophils with endothelial cells.
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6. Absence of P-selectin delays fatty streak formation in mice.
P-selectin is expressed on activated endothelium and platelets where it can bind monocytes, neutrophils, stimulated T cells, and platelets. Because recruitment of these cells is critical for atherosclerotic lesion development, we examined whether P-selectin might play a role in atherosclerosis. We intercrossed P-selectin-deficient mice with mice lacking the