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1
* Department of Internal Medicine, University of Texas Medical Branch, Galveston, TX 77555;
Shriners Burns Hospital, Galveston, TX 77550; and
University of California-Davis Medical Center, Sacramento, CA 95817
Sepsis is a major mortality concern with burned patients, who have
an increased susceptibility to infectious complications. PBMC from 41
of 45 severely burned patients (91%) failed to produce macrophage
inflammatory protein 1
(MIP-1) in cultures, while 2355–6900
pg/ml MIP-1 were produced by healthy donor PBMC, stimulation with
anti-human CD3 mAb. Healthy chimeras (SCID mice inoculated with
healthy donor PBMC) treated with anti-human MIP-1 mAb and
patient chimeras (SCID mice reconstituted with burned patient PBMC)
were susceptible (0% survival) to infectious complications induced by
well-controlled cecal ligation and puncture. In contrast, patient
chimeras treated with human recombinant MIP-1 and healthy chimeras
were resistant (
77–81% survival). Similarly, after anti-mouse
CD3 mAb stimulation, splenic mononuclear cells from burned mice (6 h to
3 days after thermal injury) did not produce significant amounts of
MIP-1 in their culture fluids. Normal mice treated with
anti-murine MIP-1 mAb and burned mice were susceptible to cecal
ligation- and puncture-induced infectious complications, while burned
mice treated with murine recombinant MIP-1 and normal mice were
resistant. Burned patients seemed to be more susceptible to infectious
complications when the production of MIP-1 was
impaired.
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