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Innate immune reactivity of the liver in rats fed a choline-deficient L-amino-acid-defined diet.

AbstractAIM:
To investigate the innate immune reactivity of tumor necrosis factor-alpha (TNF-alpha), Toll-like receptor 4 (TLR4), and CD14 in the liver of non-alcoholic steatohepatitis (NASH) model rats.
METHODS:
Male F344 rats were fed a choline-deficient L-amino-acid-defined (CDAA) diet. The rats were killed after 4 or 8 wk of the diet, and their livers were removed for immunohistochemical investigation and RNA extraction. The liver specimens were immunostained for TNF-alpha, TLR4, and CD14. The gene expressions of TNF-alpha, TLR4, and CD14 were determined by reverse-transcriptase polymerase chain reaction (RT-PCR). Kupffer cells were isolated from the liver by Percoll gradient centrifugation, and were then cultured to measure TNF-alpha production.
RESULTS:
The serum and liver levels of TNF-alpha in the CDAA-fed rats increased significantly as compared with the control group, as did the immunohistochemical values and gene expressions of TNF-alpha, TLR4, and CD14 with the progression of steatohepatitis. TNF-alpha production from the isolated Kupffer cells of the CDAA-fed rats was elevated by lipopolysaccharide stimulation.
CONCLUSION:
The expressions of TNF-alpha, TLR4, and CD14 increased in the NASH model, suggesting that TLR4 and CD14-mediated endotoxin liver damage may also occur in NASH.
AuthorsHideto Kawaratani, Tatsuhiro Tsujimoto, Toshiyuki Kitazawa, Mitsuteru Kitade, Hitoshi Yoshiji, Masahito Uemura, Hiroshi Fukui
JournalWorld journal of gastroenterology (World J Gastroenterol) Vol. 14 Issue 43 Pg. 6655-61 (Nov 21 2008) ISSN: 1007-9327 [Print] United States
PMID19034968 (Publication Type: Journal Article)
Chemical References
  • Amino Acids
  • Lipopolysaccharide Receptors
  • Tlr4 protein, rat
  • Toll-Like Receptor 4
  • Tumor Necrosis Factor-alpha
  • Alanine Transaminase
Topics
  • Alanine Transaminase (blood)
  • Amino Acids (adverse effects)
  • Animals
  • Cells, Cultured
  • Choline Deficiency (complications)
  • Disease Models, Animal
  • Fatty Liver (etiology, metabolism, pathology)
  • Immunity, Innate (physiology)
  • Kupffer Cells (metabolism, pathology)
  • Lipopolysaccharide Receptors (metabolism)
  • Liver (metabolism, pathology)
  • Male
  • Rats
  • Rats, Inbred F344
  • Toll-Like Receptor 4 (metabolism)
  • Tumor Necrosis Factor-alpha (metabolism)

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