Intra‐abdominal sepsis alters tumor necrosis factor‐α and interleukin‐1β binding to human neutrophils
作者:
H. SIMMS,
RONALD D'AMICO,
期刊:
Critical Care Medicine
(OVID Available online 1992)
卷期:
Volume 20,
issue 1
页码: 11-16
ISSN:0090-3493
年代: 1992
出版商: OVID
关键词: tumor necrosis factor;interleukins;polymorphonuclear leukocytes;sepsis;superoxide;anion;septic shock;surgery;receptors;interleukin-1β;bacterial infection
数据来源: OVID
摘要:
ObjectiveTo determine the effects of intra-abdominal sepsis on polymorphonuclear leukocyte tumor necrosis factor-α (TNF-α) and interleukin-1β (IL-1β) receptor expression.DesignProspective, randomized comparison between patients undergoing elective colon surgery vs. patients with intra-abdominal sepsis.SettingTertiary-care center with all patients with intra-abdominal sepsis in a surgical ICU environment.PatientsGroup 1 (n = 7) represents control patients who underwent elective colon surgery without intra-abdominal sepsis. Group 2 (n = 10) represents patients with intra-abdominal sepsis.Measurements and Main ResultsPolymorphonuclear leukocyte TNF-α and IL-1β receptor expression ± stimulation of the oxidative burst was measured using125I TNF-α and125I IL-1β. Superoxide anion production and candicidal activity were measured in the presence of TNF-α and IL-1β. Group 2 patients expressed fewer TNF-α and IL-1β receptors on their cell surface, and stimulation of oxidative burst reduced TNF-α and IL-1β receptor expression in group 2 more than in group 1. Diminished TNF-α and IL-1β binding reduced superoxide anion production by group 2 polymorphonuclear leukocytes. Decreased TNF-α binding but not IL-1β, reduced polymorphonuclear leukocyte candicidal activity by group 2 polymorphonuclear leukocytes.Conclusionsa) Intra-abdominal sepsis reduces polymorphonuclear leukocyte TNF-α and IL-1β receptor expression. b)Expression of these surface receptors is altered by stimulation of the polymorphonuclear leukocyte oxidative burst. c) Diminished TNF-α and IL-1β receptor expression is associated with functional impairments in polymorphonuclear leukocyte activity. (Crit Care Med 1992; 20:11)
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