Epithelial secretory responses to inflammation: Platelet activating factor and reactive oxygen metabolites

D. W. Powell

Research output: Contribution to journalArticle

12 Citations (Scopus)

Abstract

The experiments reviewed here indicate that products of immune and mast cell activation such as ROMs and PAF are capable of both directly affecting the epithelium as well as releasing other mediators, particularly prostaglandins, which act on the epithelium. A biological model is proposed in FIGURE 12. Activation of mast cells or phagocytes would release PAF and H2O2 which could directly affect the epithelium, but seem to preferentially act on other immune cells and mesenchymal cells such as endothelium and fibroblasts to release prostaglandins in proximity to the basolateral membranes of the epithelial cells and in close proximity to neurons of the submucosal plexus. Activation of the submucosal plexus by prostacyclin appears to play a major role in the alteration of electrolyte transport either induced by activation of phagocytes and mast cells, or observed with exogenous addition of H2O2 or PAF. The intestine appears to have potent mechanisms to inactivate ROMs (catalase and/or glutathione oxidase), and in the case of PAF there may be specific or nonspecific antagonists present in the intestinal lamina propria. While in high concentrations these inflammatory mediators may result in toxic damage to intestinal tissue, it would appear that in lower concentrations they may well mediate changes in electrolyte transport which could result in intestinal electrolyte and water secretion and thus diarrhoea in various states of intestinal inflammation.

Original languageEnglish (US)
Pages (from-to)232-247
Number of pages16
JournalAnnals of the New York Academy of Sciences
Volume664
DOIs
StatePublished - 1992

Fingerprint

Platelet Activating Factor
Metabolites
Mast Cells
Submucous Plexus
Electrolytes
Epithelium
Chemical activation
Phagocytes
Oxygen
Inflammation
Prostaglandins
ROM
Biological Models
Poisons
Epoprostenol
Catalase
Endothelium
Intestines
Diarrhea
Mucous Membrane

ASJC Scopus subject areas

  • Biochemistry, Genetics and Molecular Biology(all)

Cite this

Epithelial secretory responses to inflammation : Platelet activating factor and reactive oxygen metabolites. / Powell, D. W.

In: Annals of the New York Academy of Sciences, Vol. 664, 1992, p. 232-247.

Research output: Contribution to journalArticle

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abstract = "The experiments reviewed here indicate that products of immune and mast cell activation such as ROMs and PAF are capable of both directly affecting the epithelium as well as releasing other mediators, particularly prostaglandins, which act on the epithelium. A biological model is proposed in FIGURE 12. Activation of mast cells or phagocytes would release PAF and H2O2 which could directly affect the epithelium, but seem to preferentially act on other immune cells and mesenchymal cells such as endothelium and fibroblasts to release prostaglandins in proximity to the basolateral membranes of the epithelial cells and in close proximity to neurons of the submucosal plexus. Activation of the submucosal plexus by prostacyclin appears to play a major role in the alteration of electrolyte transport either induced by activation of phagocytes and mast cells, or observed with exogenous addition of H2O2 or PAF. The intestine appears to have potent mechanisms to inactivate ROMs (catalase and/or glutathione oxidase), and in the case of PAF there may be specific or nonspecific antagonists present in the intestinal lamina propria. While in high concentrations these inflammatory mediators may result in toxic damage to intestinal tissue, it would appear that in lower concentrations they may well mediate changes in electrolyte transport which could result in intestinal electrolyte and water secretion and thus diarrhoea in various states of intestinal inflammation.",
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AB - The experiments reviewed here indicate that products of immune and mast cell activation such as ROMs and PAF are capable of both directly affecting the epithelium as well as releasing other mediators, particularly prostaglandins, which act on the epithelium. A biological model is proposed in FIGURE 12. Activation of mast cells or phagocytes would release PAF and H2O2 which could directly affect the epithelium, but seem to preferentially act on other immune cells and mesenchymal cells such as endothelium and fibroblasts to release prostaglandins in proximity to the basolateral membranes of the epithelial cells and in close proximity to neurons of the submucosal plexus. Activation of the submucosal plexus by prostacyclin appears to play a major role in the alteration of electrolyte transport either induced by activation of phagocytes and mast cells, or observed with exogenous addition of H2O2 or PAF. The intestine appears to have potent mechanisms to inactivate ROMs (catalase and/or glutathione oxidase), and in the case of PAF there may be specific or nonspecific antagonists present in the intestinal lamina propria. While in high concentrations these inflammatory mediators may result in toxic damage to intestinal tissue, it would appear that in lower concentrations they may well mediate changes in electrolyte transport which could result in intestinal electrolyte and water secretion and thus diarrhoea in various states of intestinal inflammation.

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