Acute Ethanol Intoxication Suppresses E. Coli Lipopolysaccharide Enhanced Glucose Utilization by Hepatic Nonparenchymal Cells

Nympha B. D'Souza, Abraham P. Bautista, Gregory J. Bagby, Charles H. Lang, John J. Spitzer

Research output: Contribution to journalArticle

5 Citations (Scopus)

Abstract

During infection or endotoxemia, the immune system is activated and its energy needs increase. Alcohol (ETOH) intoxication on the other hand suppresses the immune system and increases susceptibility to infection. Since the liver is the primary site both for metabolism of ETOH and detoxification of bacterial lipopolysaccharides (LPS), this investigation was directed at studying the effect of acute ETOH intoxication on the LPS‐induced enhancement of in vivo glucose utilization in different types of hepatic cells. Rats were given an intravenous (IV) injection of ETOH followed by a constant infusion for 7 hr to maintain blood alcohol levels at about 175 mg/dl. E. coli LPS was administered IV at 4 hr and in vivo glucose utilization by the different types of liver cells was estimated 3 hr later using the 14C‐2‐deoxyglucose technique. Hepatocytes (HP), Kupffer (KC), and endothelial cells (EC), as well as the sequestered polymorphonuclear leukocytes (PMN), were separated from the liver by collagenasepronase digestion followed by centrifugal elutriation and Ficoll‐Hypaque density gradient centrifugation. The number of PMN in the liver was increased several‐fold 3 hr after LPS administration. The presence of ETOH did not inhibit the LPS‐induced neutrophil migration into the liver. ETOH depressed the LPS‐induced increase in glucose uptake in both EC and KC by 50 to 80%, respectively. It also reduced the LPS‐induced increase of plasma tumor necrosis factor activity by 80%. ETOH alone did not produce any significant changes in the parameters studied. Since enhanced glucose metabolism of immunologically active cells is part of the host's immune response to LPS, ETOH by suppressing this normal response may contribute to the increased susceptibility of alcoholics to infection.

Original languageEnglish (US)
Pages (from-to)249-254
Number of pages6
JournalAlcoholism: Clinical and Experimental Research
Volume15
Issue number2
DOIs
StatePublished - Jan 1 1991

Fingerprint

Liver
Escherichia coli
Lipopolysaccharides
Hepatocytes
Ethanol
Glucose
Neutrophils
Immune system
Endothelial cells
Metabolism
Immune System
Endothelial Cells
Infection
Alcohols
Alcoholic Intoxication
Detoxification
Endotoxemia
Kupffer Cells
Density Gradient Centrifugation
Centrifugation

All Science Journal Classification (ASJC) codes

  • Medicine (miscellaneous)
  • Toxicology
  • Psychiatry and Mental health

Cite this

@article{4c55f6c4072846a48a27e77c69d2d6fb,
title = "Acute Ethanol Intoxication Suppresses E. Coli Lipopolysaccharide Enhanced Glucose Utilization by Hepatic Nonparenchymal Cells",
abstract = "During infection or endotoxemia, the immune system is activated and its energy needs increase. Alcohol (ETOH) intoxication on the other hand suppresses the immune system and increases susceptibility to infection. Since the liver is the primary site both for metabolism of ETOH and detoxification of bacterial lipopolysaccharides (LPS), this investigation was directed at studying the effect of acute ETOH intoxication on the LPS‐induced enhancement of in vivo glucose utilization in different types of hepatic cells. Rats were given an intravenous (IV) injection of ETOH followed by a constant infusion for 7 hr to maintain blood alcohol levels at about 175 mg/dl. E. coli LPS was administered IV at 4 hr and in vivo glucose utilization by the different types of liver cells was estimated 3 hr later using the 14C‐2‐deoxyglucose technique. Hepatocytes (HP), Kupffer (KC), and endothelial cells (EC), as well as the sequestered polymorphonuclear leukocytes (PMN), were separated from the liver by collagenasepronase digestion followed by centrifugal elutriation and Ficoll‐Hypaque density gradient centrifugation. The number of PMN in the liver was increased several‐fold 3 hr after LPS administration. The presence of ETOH did not inhibit the LPS‐induced neutrophil migration into the liver. ETOH depressed the LPS‐induced increase in glucose uptake in both EC and KC by 50 to 80{\%}, respectively. It also reduced the LPS‐induced increase of plasma tumor necrosis factor activity by 80{\%}. ETOH alone did not produce any significant changes in the parameters studied. Since enhanced glucose metabolism of immunologically active cells is part of the host's immune response to LPS, ETOH by suppressing this normal response may contribute to the increased susceptibility of alcoholics to infection.",
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Acute Ethanol Intoxication Suppresses E. Coli Lipopolysaccharide Enhanced Glucose Utilization by Hepatic Nonparenchymal Cells. / D'Souza, Nympha B.; Bautista, Abraham P.; Bagby, Gregory J.; Lang, Charles H.; Spitzer, John J.

In: Alcoholism: Clinical and Experimental Research, Vol. 15, No. 2, 01.01.1991, p. 249-254.

Research output: Contribution to journalArticle

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T1 - Acute Ethanol Intoxication Suppresses E. Coli Lipopolysaccharide Enhanced Glucose Utilization by Hepatic Nonparenchymal Cells

AU - D'Souza, Nympha B.

AU - Bautista, Abraham P.

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AU - Spitzer, John J.

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N2 - During infection or endotoxemia, the immune system is activated and its energy needs increase. Alcohol (ETOH) intoxication on the other hand suppresses the immune system and increases susceptibility to infection. Since the liver is the primary site both for metabolism of ETOH and detoxification of bacterial lipopolysaccharides (LPS), this investigation was directed at studying the effect of acute ETOH intoxication on the LPS‐induced enhancement of in vivo glucose utilization in different types of hepatic cells. Rats were given an intravenous (IV) injection of ETOH followed by a constant infusion for 7 hr to maintain blood alcohol levels at about 175 mg/dl. E. coli LPS was administered IV at 4 hr and in vivo glucose utilization by the different types of liver cells was estimated 3 hr later using the 14C‐2‐deoxyglucose technique. Hepatocytes (HP), Kupffer (KC), and endothelial cells (EC), as well as the sequestered polymorphonuclear leukocytes (PMN), were separated from the liver by collagenasepronase digestion followed by centrifugal elutriation and Ficoll‐Hypaque density gradient centrifugation. The number of PMN in the liver was increased several‐fold 3 hr after LPS administration. The presence of ETOH did not inhibit the LPS‐induced neutrophil migration into the liver. ETOH depressed the LPS‐induced increase in glucose uptake in both EC and KC by 50 to 80%, respectively. It also reduced the LPS‐induced increase of plasma tumor necrosis factor activity by 80%. ETOH alone did not produce any significant changes in the parameters studied. Since enhanced glucose metabolism of immunologically active cells is part of the host's immune response to LPS, ETOH by suppressing this normal response may contribute to the increased susceptibility of alcoholics to infection.

AB - During infection or endotoxemia, the immune system is activated and its energy needs increase. Alcohol (ETOH) intoxication on the other hand suppresses the immune system and increases susceptibility to infection. Since the liver is the primary site both for metabolism of ETOH and detoxification of bacterial lipopolysaccharides (LPS), this investigation was directed at studying the effect of acute ETOH intoxication on the LPS‐induced enhancement of in vivo glucose utilization in different types of hepatic cells. Rats were given an intravenous (IV) injection of ETOH followed by a constant infusion for 7 hr to maintain blood alcohol levels at about 175 mg/dl. E. coli LPS was administered IV at 4 hr and in vivo glucose utilization by the different types of liver cells was estimated 3 hr later using the 14C‐2‐deoxyglucose technique. Hepatocytes (HP), Kupffer (KC), and endothelial cells (EC), as well as the sequestered polymorphonuclear leukocytes (PMN), were separated from the liver by collagenasepronase digestion followed by centrifugal elutriation and Ficoll‐Hypaque density gradient centrifugation. The number of PMN in the liver was increased several‐fold 3 hr after LPS administration. The presence of ETOH did not inhibit the LPS‐induced neutrophil migration into the liver. ETOH depressed the LPS‐induced increase in glucose uptake in both EC and KC by 50 to 80%, respectively. It also reduced the LPS‐induced increase of plasma tumor necrosis factor activity by 80%. ETOH alone did not produce any significant changes in the parameters studied. Since enhanced glucose metabolism of immunologically active cells is part of the host's immune response to LPS, ETOH by suppressing this normal response may contribute to the increased susceptibility of alcoholics to infection.

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