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Review
. 2003 Feb;7(1):23-38.
doi: 10.1186/cc1854. Epub 2002 Dec 20.

Bench-to-bedside review: functional relationships between coagulation and the innate immune response and their respective roles in the pathogenesis of sepsis

Steven M Opal  1 , Charles T Esmon
Affiliations
Review

Bench-to-bedside review: functional relationships between coagulation and the innate immune response and their respective roles in the pathogenesis of sepsis

Steven M Opal et al. Crit Care. 2003 Feb.

Abstract

The innate immune response system is designed to alert the host rapidly to the presence of an invasive microbial pathogen that has breached the integument of multicellular eukaryotic organisms. Microbial invasion poses an immediate threat to survival, and a vigorous defense response ensues in an effort to clear the pathogen from the internal milieu of the host. The innate immune system is able to eradicate many microbial pathogens directly, or innate immunity may indirectly facilitate the removal of pathogens by activation of specific elements of the adaptive immune response (cell-mediated and humoral immunity by T cells and B cells). The coagulation system has traditionally been viewed as an entirely separate system that has arisen to prevent or limit loss of blood volume and blood components following mechanical injury to the circulatory system. It is becoming increasingly clear that coagulation and innate immunity have coevolved from a common ancestral substrate early in eukaryotic development, and that these systems continue to function as a highly integrated unit for survival defense following tissue injury. The mechanisms by which these highly complex and coregulated defense strategies are linked together are the focus of the present review.

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Figures

Figure 1
Figure 1
The human Toll-like receptors and their known ligands. CpG, cytosine-phosphoryl-quanine; ECSIT, evolutionarily conserved signaling intermediate of Toll; IκB, inhibitory kappaB; IKK, IκB inducing kinase; IRAK, IL-1 receptor associated kinase; LBP-lipopolysaccharide-binding protein; LPS, lipopolysaccharide; MyD88, myeloid differentiation factor 88; NF-κB, nuclear factor-κ for B cells; NIK, NF-κB inducing kinase; PG, peptidoglycan; TIR, Toll IL-1 receptor domain; TRAF6, Tumor necrosis factor receptor associated factor-6.
Figure 2
Figure 2
The major coagulation factors and the pathways of coagulation activation in sepsis. TF, tissue factor; t-PA, tissue-type plasminogen activator.
Figure 3
Figure 3
The principal coagulation regulatory pathways and their sites of action. TF, tissue factor; t-PA, tissue-type plasminogen activator.
See this image and copyright information in PMC

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