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Eicosanoid Production in Nonparenchymal Liver Cells Isolated From Rats Infused With E. coli Endotoxin
Author(s) -
Turco E.B. Rodriguez,
Spitzer J.A.
Publication year - 1990
Publication title -
journal of leukocyte biology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.819
H-Index - 191
eISSN - 1938-3673
pISSN - 0741-5400
DOI - 10.1002/jlb.48.6.488
Subject(s) - biology , eicosanoid , extravasation , endocrinology , medicine , metabolism , kupffer cell , eicosanoid metabolism , inflammation , liver cytology , arachidonic acid , biochemistry , immunology , enzyme , liver metabolism
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‐ 14 C]‐AA. Ca 2+ ionophore A23187 (5 μM) stimulated the release of [1‐ 14 C]‐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. LTB 4 and 5‐HETE were the major metabolites accumulated in cells from rats infused with ET for 3 h, while PGD 2 played the main role in cells from saline‐infused rats. This could reflect [1‐ 14 C]‐AA metabolism by PMNP and Kupffer cells, respectively. By 30 h of ET‐infusion, a shift from PGD 2 to PGE 2 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.