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Modulation of Microbicidal Function in the Inflammatory Microenvironment

John Yee, MD; Betty Giannias; Bomi Kapadia; Louise Chartrand, RN; Nicolas V. Christou, MD, PhD, FRCSC

Arch Surg. 1994;129(1):99-105.

Abstract
Objective
To determine whether the inflammatory microenvironment primes neutrophils for increased microbicidal activity.

Design
In vitro studies of host defense were performed on surgical patients.

Setting
A tertiary care, university hospital.

Patients
A volunteer sample of hospitalized preoperative, noninfected surgical patients.

Intervention
Exudative neutrophils were collected from skin-blister chambers and functionally compared with circulating neutrophils.

Methods
Flow cytometry was used to evaluate directly neutrophil microbicidal activity (using fluoresceinated Candida albicans), formyl-methionyl-leucyl-phenylalanine (fMLP)-induced superoxide production (using 123 dihydrorhodamine), and surface expression of CDllb, CD16, and the fMLP receptor. In vitro tumor necrosis factor was used to determine the possibility and extent of further priming in both circulating and exudative neutrophils.

Results
Exudative polymorphonuclear neutrophils have enhanced microbicidal activity, superoxide production, and expression of CDllb, CD16, and the fMLP receptor. Exogenous tumor necrosis factor was able to prime circulating neutrophils but did not further augment superoxide production in exudative neutrophils.

Conclusion
The microbicidal activity of neutrophils is enhanced after exudation and is associated with neutrophil priming. The inability of exogenous tumor necrosis factor to further augment superoxide production after exudation suggests that this priming has been maximized.

(Arch Surg. 1994;129:99-105)

Author Affiliations
From the Departments of Surgery (Drs Yee and Christou and Mss Biannias, Kapadia, and Chartrand) and Microbiology (Dr Christou), Royal Victoria Hospital, McGill University, Montreal, Quebec.

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