Eicosanoid production in nonparenchymal liver cells isolated from rats infused with E. coli endotoxin

Continuous i.v. infusion of a nonlethal dose of Escherichia coll endotoxin induced an early (3‐h) accumulation of neutrophils in the rat liver followed by a later (30‐h) greater extravasation of mononuclear phagocytes (MNP). These inflammatory cells, recovered together by centrifugal elutriation, we...

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Published inJournal of leukocyte biology Vol. 48; no. 6; pp. 488 - 494
Main Authors Turco, E.B. Rodriguez, Spitzer, J.A.
Format Journal Article
LanguageEnglish
Published United States Society for Leukocyte Biology 01.12.1990
Subjects
Animals
Arachidonic Acid
arachidonic acid metabolites
Arachidonic Acids - metabolism
Calcimycin - pharmacology
Dinoprostone - biosynthesis
Eicosanoids - biosynthesis
endothelial cells
Endotoxins - toxicity
Hydroxyeicosatetraenoic Acids - biosynthesis
Kupffer cells
Leukotriene B4 - biosynthesis
Liver - metabolism
Liver - pathology
Male
neutrophils
Neutrophils - pathology
Rats
Rats, Inbred Strains
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Summary:Continuous i.v. infusion of a nonlethal dose of Escherichia coll endotoxin induced an early (3‐h) accumulation of neutrophils in the rat liver followed by a later (30‐h) greater extravasation of mononuclear phagocytes (MNP). These inflammatory cells, recovered together by centrifugal elutriation, were analyzed for their potential capacity to metabolize [1‐14C]‐AA. Ca2+ ionophore A23187 (5 μM) stimulated the release of [1‐14C]‐AA from PC and PI both in cells from saline‐ and ET‐infused rats, the latter showing a higher capacity to further metabolize AA to eicosanoids. LTB4 and 5‐HETE were the major metabolites accumulated in cells from rats infused with ET for 3 h, while PGD2 played the main role in cells from saline‐infused rats. This could reflect [1‐14C]‐AA metabolism by PMNP and Kupffer cells, respectively. By 30 h of ET‐infusion, a shift from PGD2 to PGE2 release was observed. These results suggest that eicosanoids released by nonparenchymal cells (i.e., Kupffer and endothelial cells) and PMNP in the liver of ET‐infused rats may alter the normal intercellular information flow between parenchymal and nonparenchymal cells, contributing to the severe impairment in liver function and metabolism during endotoxicosis and sepsis.
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ISSN:0741-5400
1938-3673
DOI:10.1002/jlb.48.6.488