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 CD11b, CD16, and the fMLP receptor. In vitro tumor necrosis factor alpha 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 CD11b, 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.