Expression of Human Neutrophil L-Selectin During the Systemic Inflammatory Response Syndrome Is Partly Mediated by Tumor Necrosis Factor 
Najma A. Ahmed, MD, PhD;
John Yee, MD;
Betty Giannias;
Bomi Kapadia;
Nicolas V. Christou, MD, PhD
Arch Surg. 1996;131(1):31-36.
Abstract
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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  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 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 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 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 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)
Author Affiliations
From the Department of Surgery, The Royal Victoria Hospital, McGill University, Montreal, Quebec.
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