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Article
January 1996

Expression of Human Neutrophil L-Selectin During the Systemic Inflammatory Response Syndrome Is Partly Mediated by Tumor Necrosis Factor α

Author Affiliations

From the Department of Surgery, The Royal Victoria Hospital, McGill University, Montreal, Quebec.

Arch Surg. 1996;131(1):31-36. doi:10.1001/archsurg.1996.01430130033006
Abstract

Background:  Rolling of neutrophils on the vascular endothelium is a requisite step to transmigration to areas of infection or inflammation, and this is regulated in part by the neutrophil cell adhesion molecule l-selectin.

Objectives:  To compare l-selectin expression in patients with systemic inflammatory response syndrome (SIRS) and healthy age-matched control subjects and to determine whether tumor necrosis factor α modulates l-selectin expression on human neutrophils.

Setting:  A tertiary care surgical intensive care unit at a university teaching hospital.

Subjects:  Patients identified with SIRS (American College of Critical Care Physicians and Society of Critical Care Medicine criteria) were compared with healthy age-matched control subjects. Venous blood samples that were obtained from healthy laboratory control subjects were used to examine the time course of l-selectin expression.

Main Outcome Measures:  Neutrophil l-selectin expression was determined by flow cytometry in patients with SIRS and control subjects. Tumor necrosis factor α concentrations were determined in blood and exudative fluid from patients with SIRS. Neutrophil l-selectin expression was measured during a 45-minute time course in the presence of recombinant human tumor necrosis factor α and N-formyl-methionyl-leucyl-phenylalanine.

Results:  Circulating neutrophils from patients with SIRS had significantly less l-selectin expression than did control subjects. Tumor necrosis factor α at concentrations similar to those found in exudative fluid caused a dose-and time-dependent decrease in neutrophil l-selectin expression.

Conclusion:  Tumor necrosis factor α may act as a paracrine modulator of site-specific neutrophil rolling, adhesion, and exudation via mechanisms that involve the down-regulation of l-selectin.(Arch Surg. 1996;131:31-36)

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