“Primed” Human Neutrophils on a Standard Peripheral Blood Smear

Forest R Sheppard, MD, Ernest E Moore, MD, FACS, John Ryder, MD, Alden H Harken, MD, FACS,Joao B Rezende-Neto, MD, Anirban Banerjee, MD, Christopher C Silliman, MD, PhD, University ofColorado Health Sciences Center, Denver, CO

In the two-event model of end organ injury the firstevent is the priming of circulating neutrophils (PMNs);the second stressor activates these primed PMNs withsubsequent indiscriminate release of cytotoxic reactiveoxygen metabolites and proteases into the PMN-endothelial microenvironment.1 After both trauma2 andcardiopulmonary bypass,3 circulating PMNs are primedfor superoxide release. The first “priming” event in thedevelopment of multiple organ failure can be detectedwith standard light microscopic (100�) evaluation ofroutine peripheral blood smears (Wright-Giemsa stain).The resting neutrophil (A) exhibits a smooth, round cellshape with uniform cytoplasmic granularity. After prim-ing (B), with 2�M platelet activating factor, PMNs lose

their resting morphology and exhibit an irregular cellshape and membrane, toxic granulation with polarizedgranularity (white arrowhead), and cytoplasmic vacuol-ization (black arrowhead).

REFERENCES

1. Moore FA, Moore EE. Evolving concepts in the pathogenesis ofpostinjury multiple organ failure. Surg Clin North Am 1995;75:257–277.

2. Botha AJ, Moore FA, Moore EE, et al. Postinjury neutrophilpriming and activation: An early vulnerable window. Surgery1995;118:358–364.

3. Partrick DA, Moore EE, Fullerton DA, et al. Cardiopulmonarybypass renders patients at risk for multiple organ failure via earlyneutrophil priming and later neutrophil disability. J Surg Res1999;86:42–44.

731© 2002 by the American College of Surgeons ISSN 1072-7515/02/$21.00Published by Elsevier Science Inc. PII S1072-7515(02)01301-7