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Burns. 2003 Feb;29(1):1-14.

Macrophages and post-burn immune dysfunction.

Author information

1
Center for Surgical Research, University of Alabama at Birmingham, G094 Volker Hall, 1670 University Boulevard, Birmingham, AL 35294-0019, USA. martin.schwacha@ccc.uab.edu

Abstract

The activation of a pro-inflammatory cascade after burn injury appears to be important in the development of subsequent immune dysfunction, susceptibility to sepsis and multiple organ failure. Macrophages are major producers of pro-inflammatory mediators and their productive capacity for these mediators is markedly enhanced following thermal injury. Thus, macrophage hyperactivity (as defined by increased productive capacity for pro-inflammatory mediators) appears to be of critical importance in the development of post-burn immune dysfunction. This review will focus on the current state of knowledge with regards to the role of macrophages in the development of post-burn immune dysfunction. Particular areas of discussion include: nitric oxide synthase (NOS) and cyclooxygenase (COX) enzyme systems, macrophages and the T-helper (Th)-1/Th-2 cytokine responses, alterations in macrophages signal transduction and a potential role for gamma/delta T-cells in the development of macrophage hyperactivity following thermal injury. A more comprehensive understanding of the relationship between macrophage activity and post-burn immune dysfunction will hopefully provide the basis for improved therapeutic regimes in the treatment of burn patients.

PMID:
12543039
DOI:
10.1016/s0305-4179(02)00187-0
[Indexed for MEDLINE]

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