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Neutrophils from patients after burn injury express a deficiency of the
oxidase components p47-phox and p67-phox
J Rosenthal, GW Thurman, N Cusack, VM Peterson, HL Malech and DR Ambruso
Department of Pediatrics, University of Colorado School of Medicine,
Denver, USA.
Infection is a major cause of morbidity and mortality in patients after
thermal injury. This predisposition to infections is related, in part, to
abnormal polymorphonuclear leukocyte (PMN) function and a diminished
respiratory burst. To evaluate the biochemical basis for the defective
respiratory burst after major burns, the status of the oxidase enzyme
system and its components was investigated. PMNs were isolated from 24
patients with 12% to 62% burns. Oxidase activity of intact PMNs, measured
as superoxide anion (O2-) generation or oxygen consumption, was decreased
in burn compared with healthy controls. Subcellular fractions from patient
PMNs generated less O2- in the sodium dodecyl sulfate cell-free system, and
this was related to a diminished contribution by cytosol but not by plasma
membrane. Subsequently, cytosol was separated with CM-Sepharose, yielding
two fractions; one contained the p47-phox and p67-phox (47/67 mix) and the
other contained the remaining cytosolic components (run through [RT]).
Although the contribution to oxidase activity made by RT from patient
cytosol was similar to that of control, the activity of p47/67 mix from
PMNs of burn patients was deficient. Quantitative assays using an
immunoautoradiographic technique showed a consistent, but significant
decrease in both p47-phox and p67-phox. The addition of purified or human
recombinant p47-phox but not p67-phox corrected the diminished oxidase
activity of cytosol from burn patients. Thus, decreased respiratory burst
activity found in PMNs from individuals with thermal injury was associated
with a specific, quantitative deficiency of p47- phox.
Volume 88,
Issue 11,
pp. 4321-4329,
12/01/1996
Copyright © 1996 by The American Society of Hematology
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