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A Potential Mechanism for Control of Neutrophil Superoxide Production in Sepsis

Joseph S. Solomkin, MD; Julia K. Brodt; Frank P. Zemlan, PhD

Arch Surg. 1986;121(1):77-80.

Abstract
• Previous studies with neutrophils from patients with intraabdominal sepsis have provided convincing evidence of in vivo exposure to C5a. However, in contradistinction to normal cells pretreated with C5a, patient cells showed depressed superoxide response to N-formyl-methionyl-leucyl-phenylalanine (FMLP) and enhanced FMLP receptor affinity. To identify possible mechanisms responsible for these findings, we examined the effects of lysosomal alkalinization with the weak base clindamycin on normal neutrophils with and without C5a. Our results showed a specific suppression of FMLP-induced superoxide production and a loss of low-affinity FMLP receptors. These results occurred in the presence of clindamycin levels that did not interfere with other cellular processes. These findings suggest that regulation of neutrophil function during the course of intra-abdominal sepsis may be due to effectors active both at the cell surface (C5a) and within the lysosome. The clinical significance of our findings relates to a possible mechanism for specific pharmacologic suppression of oxide-radical production by neutrophils. Such oxide radicals are believed to be important in the capillary injury accompanying severe sepsis.

(Arch Surg 1986;121:77-80)

Author Affiliations
From the Departments of Surgery (Dr Solomkin and Ms Brodt) and Psychiatry (Dr Zemlan), University of Cincinnati College of Medicine.

Footnotes
Accepted for publication Sept 5, 1985.

Read before the Fifth Annual Meeting of the Surgical Infection Society, New Orleans, April 29, 1985.

Reprint requests to Department of Surgery, University of Cincinnati College of Medicine, ML#558, 231 Bethesda Ave, Cincinnati, OH 45267-0558 (Dr Solomkin).

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