Lipopolysaccharide is a cofactor for malondialdehyde-acetaldehyde adduct-mediated cytokine/chemokine release by rat sinusoidal liver endothelial and Kupffer cells

Michael J. Duryee, Lynell W. Klassen, Thomas L. Freeman, Monte Willis, Dean J. Tuma, Geoffrey M. Thiele

Research output: Contribution to journalArticle

47 Citations (Scopus)

Abstract

Background: The nonparenchymal cells of the liver have been suggested to play a significant role in the inflammatory processes observed in the development and/or progression of alcoholic liver disease. Our laboratories have shown that malondialdehyde-acetaldehyde (MAA)-modified proteins can induce immune responses, cytokine/chemokine secretion, and antigen processing and presentation by liver sinusoidal endothelial cells (SECs). Another molecule that has been shown to induce similar types of responses in Kupffer cells (KCs) is lipopolysaccharide (LPS). Because these materials induce similar responses, it was the purpose of this study to investigate the relationship between LPS and MAA-modified proteins in the development of proinflammatory responses by SECs and KCs. Methods: For these studies, SECs and KCs were isolated from chow-fed, pair-fed, and ethanol-fed rats. Cells were stimulated with media alone, bovine serum albumin (Alb), or MAA-modified Alb (MAA-Alb) in the presence or absence of LPS 1 ng/ml, and the supernatants were assayed by enzyme-linked immunosorbent assay for tumor necrosis factor a, macrophage chemotactic protein 1, and macrophage inhibitory protein. Results: All three cytokines/chemokines were 3 to 5 times higher when SECs or KCs were stimulated by MAA-Alb in the presence of LPS, in contrast to cells stimulated with Alb or media in the presence of LPS. Chronic ethanol consumption (6 weeks) had variable effects on the secretion of these cytokines/chemokines but in general did not alter the increased secretion in response to MAA-Alb in the presence of LPS. Conclusions: These studies strongly suggest that the sensitization of SECs and KCs by LPS plays a significant role in the development and/or progression of alcoholic liver disease, and the subsequent activation by MAA-modified proteins may be a mechanism by which proinflammatory processes are initiated.

Original languageEnglish (US)
Pages (from-to)1931-1938
Number of pages8
JournalAlcoholism: Clinical and Experimental Research
Volume28
Issue number12
DOIs
StatePublished - Dec 1 2004
Externally publishedYes

Fingerprint

Kupffer Cells
Acetaldehyde
Endothelial cells
Malondialdehyde
Chemokines
Liver
Lipopolysaccharides
Rats
Endothelial Cells
Cytokines
Albumins
Alcoholic Liver Diseases
Macrophages
Antigen Presentation
Proteins
Ethanol
Immunosorbents
Bovine Serum Albumin
Assays
Tumor Necrosis Factor-alpha

Keywords

  • Adducts
  • Aldehydes
  • Kupffer Cells
  • LPS
  • Scavenger Receptors

ASJC Scopus subject areas

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

Cite this

Lipopolysaccharide is a cofactor for malondialdehyde-acetaldehyde adduct-mediated cytokine/chemokine release by rat sinusoidal liver endothelial and Kupffer cells. / Duryee, Michael J.; Klassen, Lynell W.; Freeman, Thomas L.; Willis, Monte; Tuma, Dean J.; Thiele, Geoffrey M.

In: Alcoholism: Clinical and Experimental Research, Vol. 28, No. 12, 01.12.2004, p. 1931-1938.

Research output: Contribution to journalArticle

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T1 - Lipopolysaccharide is a cofactor for malondialdehyde-acetaldehyde adduct-mediated cytokine/chemokine release by rat sinusoidal liver endothelial and Kupffer cells

AU - Duryee, Michael J.

AU - Klassen, Lynell W.

AU - Freeman, Thomas L.

AU - Willis, Monte

AU - Tuma, Dean J.

AU - Thiele, Geoffrey M.

PY - 2004/12/1

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N2 - Background: The nonparenchymal cells of the liver have been suggested to play a significant role in the inflammatory processes observed in the development and/or progression of alcoholic liver disease. Our laboratories have shown that malondialdehyde-acetaldehyde (MAA)-modified proteins can induce immune responses, cytokine/chemokine secretion, and antigen processing and presentation by liver sinusoidal endothelial cells (SECs). Another molecule that has been shown to induce similar types of responses in Kupffer cells (KCs) is lipopolysaccharide (LPS). Because these materials induce similar responses, it was the purpose of this study to investigate the relationship between LPS and MAA-modified proteins in the development of proinflammatory responses by SECs and KCs. Methods: For these studies, SECs and KCs were isolated from chow-fed, pair-fed, and ethanol-fed rats. Cells were stimulated with media alone, bovine serum albumin (Alb), or MAA-modified Alb (MAA-Alb) in the presence or absence of LPS 1 ng/ml, and the supernatants were assayed by enzyme-linked immunosorbent assay for tumor necrosis factor a, macrophage chemotactic protein 1, and macrophage inhibitory protein. Results: All three cytokines/chemokines were 3 to 5 times higher when SECs or KCs were stimulated by MAA-Alb in the presence of LPS, in contrast to cells stimulated with Alb or media in the presence of LPS. Chronic ethanol consumption (6 weeks) had variable effects on the secretion of these cytokines/chemokines but in general did not alter the increased secretion in response to MAA-Alb in the presence of LPS. Conclusions: These studies strongly suggest that the sensitization of SECs and KCs by LPS plays a significant role in the development and/or progression of alcoholic liver disease, and the subsequent activation by MAA-modified proteins may be a mechanism by which proinflammatory processes are initiated.

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