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Francis D. Moore, Jr, MD; Susan H. Socher, PhD; Carl Davis, MCh, FRSC(I)

Arch Surg. 1991;126(1):70-73.

Abstract
• We investigated the possibility that tumor necrosis factor (TNF) mediates neutrophil activation by endotoxin. The number of C3b receptors on the neutrophil cell-surface was used as the indicator of activation, as assessed by indirect immunofluorescence. Incubation of buffy-coat neutrophils with TNF- for 30 minutes at 37°C caused neutrophil activation, increasing C3b receptor–dependent fluorescence from 340 with buffer alone to 580 with TNF (250 pg/mL). Increasing amounts of anti-TNF IgG progressively inhibited neutrophil activation by TNF (250 pg/mL). Addition of the active dose range of anti-TNF to neutrophils incubating in endotoxin (10 ng/mL) did not affect the degree of endotoxin-mediated neutrophil activation. Mixtures of neutrophils with the 50% suppressive dose of anti-TNF and varying endotoxin concentrations showed the same degree of neutrophil activation as mixtures without the antibody. Thus, an antibody that can inhibit TNF-mediated neutrophil activation does not inhibit endotoxin-mediated neutrophil activation. We conclude that endotoxin and TNF can activate neutrophils through separate pathways.

(Arch Surg. 1991;126:70-73)

Author Affiliations
From the Department of Surgery, Harvard Medical School, Brigham and Women's Hospital, Boston, Mass (Drs Moore and Davis); and the Department of Pharmacology, Merck Sharp & Dohme Research Laboratories, West Point, Pa (Dr Socher).

Footnotes
Accepted for publication September 29, 1990.

Read before the Tenth Anniversary Meeting of the Surgical Infection Society, Cincinnati, Ohio, June 15, 1990.

Reprint requests to 75 Francis St, Boston, MA 02115 (Dr Moore).

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