An increase in the susceptibility of burned patients to infectious complications due to impaired production of macrophage inflammatory protein 1α1

Makiko Kobayashi, Hitoshi Takahashi, Arthur P. Sanford, David N. Herndon, Richard B. Pollard, Fujio Suzuki

Research output: Contribution to journalArticle

39 Scopus citations

Abstract

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 1α (MIP-1α) in cultures, while 2355-6900 pg/ml MIP-1α 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-1α 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-1α 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-1α in their culture fluids. Normal mice treated with anti-murine MIP-1α mAb and burned mice were susceptible to cecal ligation- and puncture-induced infectious complications, while burned mice treated with murine recombinant MIP-1α and normal mice were resistant. Burned patients seemed to be more susceptible to infectious complications when the production of MIP-1α was impaired.

Original languageEnglish (US)
Pages (from-to)4460-4466
Number of pages7
JournalJournal of Immunology
Volume169
Issue number8
StatePublished - Oct 15 2002

ASJC Scopus subject areas

  • Immunology and Allergy
  • Immunology

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    Kobayashi, M., Takahashi, H., Sanford, A. P., Herndon, D. N., Pollard, R. B., & Suzuki, F. (2002). An increase in the susceptibility of burned patients to infectious complications due to impaired production of macrophage inflammatory protein 1α1. Journal of Immunology, 169(8), 4460-4466.