Effect of critical illness on microbial translocation and gastrointestinal mucosa permeability
- PMID: 7886323
Effect of critical illness on microbial translocation and gastrointestinal mucosa permeability
Abstract
It has been hypothesized that the barrier function of the gastrointestinal tract is deranged in patients with trauma, sepsis, or other critical illnesses. Derangements in intestinal barrier function might lead to bloodstream invasion by gut-derived microbes and/or activation of inflammatory cells in the submucosa of the intestine or within the liver. Activated immune cells are capable of releasing a number of inflammatory mediators, including eicosanoids and cytokines, which have been implicated in the pathogenesis of the multiple organ dysfunction syndrome (MODS). Thus, gut-barrier dysfunction might be primary factor leading to MODS in patients with critical illness. Two distinct forms of gut-barrier dysfunction have been described. The first, called translocation, appears to a transcellular process, whereby particulate antigens, including viable microbes, are transported across enterocytes into the submucosal compartment. The second is an increase in the paracellular permeability of the intestinal epithelium, which permits increased transmucosal absorption of water-soluble macromolecules. Pathological increases in both translocation and permeability occur in a number of animal models of critical illness. Moreover, a number of studies have documented that intestinal permeability is increased in humans with trauma, sepsis, burns, or other serious, acute medical problems. Nevertheless, convincing data to establish a causal link between gut-barrier dysfunction and organ failure in humans are lacking, and the importance of translocation and/or mucosal hyperpermeability on the development of MODS in patients remains to be elucidated.
Similar articles
-
Infection, the gut and the development of the multiple organ dysfunction syndrome.Eur J Surg. 1996 Apr;162(4):259-73. Eur J Surg. 1996. PMID: 8739412 Review.
-
Gut dysfunction in critically ill patients: a review of the literature.Am J Crit Care. 1997 May;6(3):204-9. Am J Crit Care. 1997. PMID: 9131199 Review.
-
[Microbial translocation from the gastrointestinal tract--pathophysiologic phenomenon or catalyst for multiple organ failure?].Zentralbl Chir. 1994;119(4):256-67. Zentralbl Chir. 1994. PMID: 8203177 Review. German.
-
The relationship between gut-derived bacteria and the development of the multiple organ dysfunction syndrome.J Anat. 1996 Dec;189 ( Pt 3)(Pt 3):537-48. J Anat. 1996. PMID: 8982828 Free PMC article. Review.
-
[Gastrointestinal tract dysfunction in critical illness].Cas Lek Cesk. 2002 Feb 1;141(2):46-50. Cas Lek Cesk. 2002. PMID: 11925662 Review. Czech.
Cited by
-
Bacterial translocation in surgical patients.Ann R Coll Surg Engl. 1997 May;79(3):183-9. Ann R Coll Surg Engl. 1997. PMID: 9196338 Free PMC article. Review. No abstract available.
-
The adenosine deaminase inhibitor erythro-9-[2-hydroxyl-3-nonyl]-adenine decreases intestinal permeability and protects against experimental sepsis: a prospective, randomised laboratory investigation.Crit Care. 2008;12(5):R125. doi: 10.1186/cc7033. Epub 2008 Oct 13. Crit Care. 2008. PMID: 18847498 Free PMC article.
-
Orexigenic hormone ghrelin attenuates local and remote organ injury after intestinal ischemia-reperfusion.PLoS One. 2008 Apr 23;3(4):e2026. doi: 10.1371/journal.pone.0002026. PLoS One. 2008. PMID: 18431503 Free PMC article.
-
Clostridium difficile infection as a cause of severe sepsis.Intensive Care Med. 1996 Sep;22(9):990-4. doi: 10.1007/BF02044130. Intensive Care Med. 1996. PMID: 8905440
-
Reversing established sepsis in rats with human vasoactive hormone adrenomedullin and its binding protein.Mol Med. 2009 Jan-Feb;15(1-2):28-33. doi: 10.2119/molmed.2008.00092. Epub 2008 Oct 10. Mol Med. 2009. PMID: 19009024 Free PMC article.
Publication types
MeSH terms
LinkOut - more resources
Other Literature Sources