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Titolo:
Effects in humans of intravenously administered endotoxin on soluble cell-adhesion molecule and inflammatory markers: A model of human diseases
Autore:
Wilson, MF; Blum, R; Dandona, P; Mousa, SA;
Indirizzi:
DuPont Pharmaceut Co, Expt Stn E400 3470, Wilmington, DE 19880 USA DuPont Pharmaceut Co Wilmington DE USA 19880 70, Wilmington, DE 19880 USA Kaleida Hlth, Dept Cardiol, Buffalo, NY USA Kaleida Hlth Buffalo NY USAKaleida Hlth, Dept Cardiol, Buffalo, NY USA Kaleida Hlth, Dept Endocrinol, Buffalo, NY USA Kaleida Hlth Buffalo NY USA leida Hlth, Dept Endocrinol, Buffalo, NY USA SUNY Buffalo, Buffalo, NY 14260 USA SUNY Buffalo Buffalo NY USA 14260SUNY Buffalo, Buffalo, NY 14260 USA
Titolo Testata:
CLINICAL AND EXPERIMENTAL PHARMACOLOGY AND PHYSIOLOGY
fascicolo: 5-6, volume: 28, anno: 2001,
pagine: 376 - 380
SICI:
0305-1870(200105/06)28:5-6<376:EIHOIA>2.0.ZU;2-0
Fonte:
ISI
Lingua:
ENG
Soggetto:
TUMOR-NECROSIS-FACTOR; SEPTIC SHOCK; FACTOR-ALPHA; INHIBITION; RESPONSES; KINETICS;
Keywords:
endothelial cell; endotoxin; inflammatory markers; leucocyte; platelet; soluble adhesion molecules; tumour necrosis factor-alpha; tumour necrosis factor soluble receptor;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
32
Recensione:
Indirizzi per estratti:
Indirizzo: Mousa, SA DuPont Pharmaceut Co, Expt Stn E400 3470, 141 Henry Clay Rd, Wilmington, DE 19880 USA DuPont Pharmaceut Co 141 Henry Clay Rd Wilmington DE USA 19880 A
Citazione:
M.F. Wilson et al., "Effects in humans of intravenously administered endotoxin on soluble cell-adhesion molecule and inflammatory markers: A model of human diseases", CLIN EXP PH, 28(5-6), 2001, pp. 376-380

Abstract

1. Endotoxin, a component of the cell wall of Gram-negative bacteria, could be a predisposing mediator of many pathological disorders. The present study was undertaken to determine the effects and time-course of acute endotoxin challenge on inflammatory and cell-adhesion molecule markers shedding in the plasma as potential surrogates.2. Six normal male subjects per group (age range 21-35 years) were injected with 4 ng/kg, i.v., reference standard Escherichia coli (0113:h10:k) endotoxin or physiological saline.3. Plasma inflammatory markers (tumour necrosis factor (TNF)-alpha, interleukin (IL)-6 and TNF-receptor I (RI)) and cell-adhesion molecule markers (soluble L-selectin, soluble P-selectin, soluble vascular cell adhesion molecule (VCAM)-1) were determined using sensitive and specific ELISA.4. Tumour necrosis factor-alpha increased from a basal level of 2.8 pg/mL to approximately 800 pg/mL at 90 min after endotoxin. Similarly, IL-6 peaked 2-3 h after endotoxin injection, with a rapid decline by 6-8 h, and levels returned to basal values by 24 h.5. In contrast, TNF-RI peaked at 2 h (increasing from basal levels of 900-3300 pg/mL) with a much slower decline and without return to basal levels at 24 h (1400 pg/mL).6. Endotoxin resulted in a rapid rise in soluble L-selectin within 1 h, which increased from a basal of 150-425 ng/mL. This rapid rise in soluble L-selectin was sustained for up to 2.5 h and then rapidly declined to basal levels by 3.5 h.7. In contrast, plasma soluble P-selectin levels showed a delayed and progressive increase up to 8 h (increasing from a basal level of 50-95 ng/mL), with a partial decline at 24 h (80 ng/mL).8. Similarly, soluble VCAM-1 levels showed a progressive rise up to 24 h (increasing from basal values of 600-1000 ng/mL).9. This acute human model of endotoxin exposure demonstrated an upregulation of inflammatory stimuli leading to a short-term hyperactivation of leucocytes and a more sustained activation of platelets and endothelium.10. This model provides a non-invasive method for studying the complex effects of endotoxin-like pathogens on different cellular events using solubleplasma surrogate markers.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 23/10/20 alle ore 12:01:53