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Review
. 2007 Oct;28(4):384-93.
doi: 10.1097/shk.0b013e31805569df.

Intestinal crosstalk: a new paradigm for understanding the gut as the "motor" of critical illness

Jessica A Clark  1 , Craig M Coopersmith
Affiliations
Review

Intestinal crosstalk: a new paradigm for understanding the gut as the "motor" of critical illness

Jessica A Clark et al. Shock. 2007 Oct.

Abstract

For more than 20 years, the gut has been hypothesized to be the "motor" of multiple organ dysfunction syndrome. As critical care research has evolved, there have been multiple mechanisms by which the gastrointestinal tract has been proposed to drive systemic inflammation. Many of these disparate mechanisms have proved to be important in the origin and propagation of critical illness. However, this has led to an unusual situation where investigators describing the gut as a "motor" revving the systemic inflammatory response syndrome are frequently describing wholly different processes to support their claim (i.e., increased apoptosis, altered tight junctions, translocation, cytokine production, crosstalk with commensal bacteria, etc). The purpose of this review is to present a unifying theory as to how the gut drives critical illness. Although the gastrointestinal tract is frequently described simply as "the gut," it is actually made up of (1) an epithelium; (2) a diverse and robust immune arm, which contains most of the immune cells in the body; and (3) the commensal bacteria, which contain more cells than are present in the entire host organism. We propose that the intestinal epithelium, the intestinal immune system, and the intestine's endogenous bacteria all play vital roles driving multiple organ dysfunction syndrome, and the complex crosstalk between these three interrelated portions of the gastrointestinal tract is what cumulatively makes the gut a "motor" of critical illness.

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Figures

Figure 1
Figure 1
Crosstalk between the intestinal epithelium, immune system, and commensal bacteria is central to initiating the systemic inflammatory response. We hypothesize that the cumulative and integrated result of these multiple interactions is what makes the gut the “motor” of critical illness.
Figure 2
Figure 2
The intestinal barrier. The epithelium, immune cells, and commensal bacteria work together to prevent invasion of potentially harmful substances.
See this image and copyright information in PMC

References

    1. Carrico CJ, Meakins JL, Marshall JC, Fry D, Maier RV. Multiple-organ-failure syndrome. The gastrointestinal tract: the "motor" of MOF. Arch Surg. 1986;121:196–208. - PubMed
    1. American College of Chest Physicians/Society of Critical Care Medicine Consensus Conference: definitions for sepsis and organ failure and guidelines for the use of innovative therapies in sepsis. Crit Care Med. 1992;20:864–874. - PubMed
    1. Hassoun HT, Kone BC, Mercer DW, Moody FG, Weisbrodt NW, Moore FA. Post-injury multiple organ failure: the role of the gut. Shock. 2001;15:1–10. - PubMed
    1. Fink MP. Intestinal epithelial hyperpermeability: update on the pathogenesis of gut mucosal barrier dysfunction in critical illness. Curr Opin Crit Care. 2003;9:143–151. - PubMed
    1. Han X, Fink MP, Yang R, Delude RL. Increased iNOS activity is essential for intestinal epithelial tight junction dysfunction in endotoxemic mice. Shock. 2004;21:261–270. - PubMed

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