Tumor necrosis factor stimulates amino acid transport in plasma membrane vesicles from rat liver.

Pacitti, Anthony J.; Inoue, Yasuhiro; Souba, Wiley W.

doi:10.1172/jci116225

Cited by 53 publications

(16 citation statements)

References 33 publications

(48 reference statements)

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“…TNF-α has been shown to exhibit a permissive effect in enhancing the stimulation of amino acid transport by glucagon [34]. The marked increase in Na + -dependent amino acid transport by TNF-α in i o is, in part, mediated by glucocorticoids [35]. Alanine transport in hepatic membrane vesicles has also been reported to be stimulated in endotoxin-treated rats [36].…”

Section: Discussionmentioning

confidence: 99%

Administration of Escherichia coli endotoxin to rat increases liver mass and hepatocyte volume in vivo

Qian

Brosnan²

1996

Biochemical Journal

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We have established, in vivo, an increase in liver mass and hepatocyte volume after a single intraperitoneal administration, to fasted rats, of Escherichia coli lipopolysaccharide (0127:B8) at 3 mg/kg. The phenomenon was time- and dose-dependent and could be prevented by treatment with polyclonal antiserum against tumour necrosis factor-α (TNF-α) before the endotoxin injection. Endotoxin caused an increase of 26% in the hepatic mass compared with fasted controls at 24 h. An increase of 27% in the hepatic water content underlay the altered hepatic mass which could not be accounted for by a change in the volume of hepatic blood and/or interstitial fluid (measured in vivo), suggesting an expansion in the hepatocellular volume. This is supported by an increase of 25% in the K+ content of the endotoxic livers. Morphometric study confirmed a 15% increase in hepatocyte volume after endotoxin administration. The data are discussed in the light of possible metabolic effects of increased hepatocyte volume.

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Section: Discussionmentioning

confidence: 99%

Administration of Escherichia coli endotoxin to rat increases liver mass and hepatocyte volume in vivo

Qian

Brosnan²

1996

Biochemical Journal

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“…Treatment with TNF-α has also been shown not to produce any effect on the activity of ecto-ATPase (Pacitti et al 1993). Moreover, it has recently been demonstrated that Spgp, rather than ectoATPase, is the major driving force of bile salt transport across the canalicular membrane (Gerloff et al 1998).…”

Section: Introductionmentioning

confidence: 99%

Lipopolysaccharide alters ecto-ATP-diphosphohydrolase and causes relocation of its reaction product in experimental intrahepatic cholestasis

Zinchuk

Okada

Seguchi

2001

Cell and Tissue Research

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Lipopolysaccharide (LPS), a bacterial endotoxin, exerts profound inflammatory actions toward various tissues and cells. We induced intrahepatic cholestasis in rats by administration of LPS and followed ecto-ATP-diphosphohydrolase (ecto-apyrase) activity in the liver. The activity of the enzyme had decreased to 77% 2 h after injection compared with the activity in control animals. The maximum decrease was detected 24 h after administration. The activity was found to have partially recovered 1 week after injection, but had yet to reach control levels. In contrast to the decrease in ecto-apyrase activity, there were increases in alkaline phosphatase activity and bilirubin concentration, markers of cholestasis. In response to LPS, the reaction product of ecto-apyrase was found to relocate from the canalicular domain of the plasma membrane of hepatocytes, its predominant localization in the liver of intact animals, to the basolateral and sinusoidal domains. The pattern of histochemical reaction indicated modulation of the enzyme activity and changes in trafficking of intracellular proteins. Taken together, our findings showed that LPS administration alters ecto-apyrase and causes relocation of its reaction product from the canalicular domain of the plasma membrane of hepatocytes in the rat. It is suggested that relocation of the reaction product may be a protective mechanism to enable the hepatocytes to withstand the cytokine-induced metabolic perturbations.

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“…Since there was evidence for an increase in alveolar epithelial liquid clearance, the second objective was to study the mechanism by administering amiloride, a sodium transport inhibitor, and propranolol, a beta-adrenergic antagonist, into the distal airspaces of the rats with pneumonia. Although TNF ␣ has been reported to play a role in increased lung epithelial permeability in acute lung injury (13), TNF ␣ has also been reported to increase sodium-dependent amino acid transport in rat hepatocytes (14). Therefore, our third objective was to test the hypothesis that TNF ␣ mediates the bacterially induced increase in alveolar fluid clearance.…”

Section: Introductionmentioning

confidence: 99%

“…Some experimental studies implicate TNF␣ in the increase of lung endothelial or epithelial permeability (13,48). However, it is also known that TNF␣ can increase sodium-dependent amino acid transport in rat hepatocytes (14). Therefore, our third objective was to test the hypothesis that TNF␣ could mediate the increase in alveolar fluid clearance in this 24-h model of severe bacterial pneumonia.…”

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confidence: 99%

Acute bacterial pneumonia in rats increases alveolar epithelial fluid clearance by a tumor necrosis factor-alpha-dependent mechanism.

Rezaiguia¹,

Garat²,

Delclaux³

et al. 1997

J. Clin. Invest.

159

118

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To study the rate and regulation of alveolar fluid clearance in acute pneumonia, we created a model of Pseudomonas aeruginosa pneumonia in rats. To measure alveolar liquid and protein clearance, we instilled into the airspaces a 5% bovine albumin solution with 1.5 Ci of 125 I-human albumin, 24 h after intratracheal instillation of bacteria. The concentration of unlabeled and labeled protein in the distal airspaces over 1 h was used as an index of net alveolar fluid clearance. Since there was histologic evidence of alveolar epithelial injury, several methods were used to measure alveolar fluid clearance, including the use of experiments in rats with blood flow and the use of experiments in rats without blood flow, so that movement across the epithelial barrier would be minimized in the latter group. The results with each method were identical. We found that P. aeruginosa pneumonia increased alveolar liquid clearance over 1 h by 48% in studies with blood flow, and by 43% in rats without blood flow, compared with respective controls ( P Ͻ 0.05). In both studies, this increase was inhibited with amiloride. However, propranolol had no inhibitory effect, thus ruling out a catecholamine-dependent mechanism to explain the increase in alveolar fluid clearance. An antitumor necrosis factor-␣ neutralizing antibody, instilled into the lung 5 min before bacteria, prevented the increase in alveolar liquid clearance in rats with pneumonia ( P Ͻ 0.05). Also, TNF ␣ (5 g) instilled in normal rats increased alveolar liquid clearance by 43% over 1 h compared with control rats ( P Ͻ 0.05). In normal rats instilled with TNF ␣ , propranolol had no inhibitory effect. In conclusion, gram-negative pneumonia markedly upregulates net alveolar epithelial fluid clearance, in part by a TNF ␣ -dependent mechanism. This finding provides a novel mechanism for the upregulation of alveolar epithelial sodium and fluid transport from the distal airspaces of the lung. ( J. Clin. Invest. 1997. 99:325-335.)

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Tumor necrosis factor stimulates amino acid transport in plasma membrane vesicles from rat liver.

Cited by 53 publications

References 33 publications

Administration of Escherichia coli endotoxin to rat increases liver mass and hepatocyte volume in vivo

Administration of Escherichia coli endotoxin to rat increases liver mass and hepatocyte volume in vivo

Lipopolysaccharide alters ecto-ATP-diphosphohydrolase and causes relocation of its reaction product in experimental intrahepatic cholestasis

Acute bacterial pneumonia in rats increases alveolar epithelial fluid clearance by a tumor necrosis factor-alpha-dependent mechanism.

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