Thermal injury-induced immunosuppression in mice: The role of macrophage-derived reactive nitrogen intermediates

Martin G. Schwacha, Scott D. Somers

Research output: Contribution to journalArticlepeer-review

72 Scopus citations

Abstract

Macrophages (Mφ) have been implicated in the suppression of lymphocyte function following thermal injury. Splenocytes isolated from C57BL/6NCR female mice 4-7 days after thermal injury displayed suppressed proliferative responses to Concanavalin A (ConA) and lipopolysaccharide (LPS) and high levels of reactive nitrogen intermediate (RNI) production. Inhibition of nitric oxide synthase activity with N(G)-monomethyl-L-arginine restored ConA responses but not LPS responses. Surprisingly, ConA-stimulated interferon-γ (IFN-γ) production was increased in splenocytes from injured mice. IFN-γ contributed to the RNI-mediated immunosuppression as antibodies against IFN- γ reduced RNI production and immunosuppression. ConA-stimulated co-cultures of splenic Mφ from injured mice and normal splenocytes produced high levels of RNI only under conditions of cellular contact and splenic mφ from injured mice were capable of suppressing normal splenocytes responses in co-culture. These results indicate that Mφ activity and specifically RNI production contribute to the suppression of T lymphocyte function after thermal injury.

Original languageEnglish (US)
Pages (from-to)51-58
Number of pages8
JournalJournal of Leukocyte Biology
Volume63
Issue number1
DOIs
StatePublished - 1998

Keywords

  • Burn
  • Inducible nitric oxide synthase
  • Interferon-γ
  • Nitric oxide
  • T lymphocyte
  • Trauma

ASJC Scopus subject areas

  • Immunology and Allergy
  • Immunology
  • Cell Biology

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