Differential expression of cytokine genes in monocytes, peritoneal macrophages and liver following endotoxin- or turpentine-induced inflammation in rat

• Published in: Cytokine (Philadelphia, Pa.) Pa.), 1996-02, Vol.8 (2), p.115-120
• Main Authors: Scotté, M., Hiron, M., Masson, S., Lyoumi, S., Banine, F., Ténière, P., Lebreton, J.P., Daveau, M.
• Format: Article
• Language: English
• Subjects: Animals; Base Sequence; Cytokine; Cytokines - genetics; endotoxaemia; Gene Expression Regulation - drug effects; inflammation; Inflammation - chemically induced; Inflammation - metabolism; Injections, Intraperitoneal; Injections, Intravenous; Lipopolysaccharides; Liver - cytology; Liver - drug effects; Liver - metabolism; Macrophages, Peritoneal - drug effects; Macrophages, Peritoneal - metabolism; Male; Molecular Sequence Data; Monocytes - drug effects; Monocytes - metabolism; Rats; Rats, Sprague-Dawley; RT-PCR; Turpentine
• ISSN: 1043-4666; 1096-0023
• DOI: 10.1006/cyto.1996.0016

Pro-inflammatory cytokines are produced after systemic or local inflammation by a wide variety of cell types including monocytes, macrophages, Kupffer and endothelial cells. Previous studies have shown that IL-6 gene expression does not occur in liver from rats undergoing an acute phase response after turpentine injection or controls. These data do not rule out the possibility that delivery of a pathogen to the liver via the portal circulation could directly activate the Kupffer cells. Rats were injected either intravenously or intraperitoneally with LPS, or subcutaneously with turpentine oil. The changes in IL-1β, IL-6, and TNF mRNA levels in monocytes (collected from portal vein or caval cein), peritoneal macrophages and liver over a 3-hour period post-treatment were examined. The kinetics of LPS- vs turpentine-induced cytokine mRNAs in these various cell types were compared by quantitative reverse transcription and polymerase chain reaction (RT-PCR). Our data demonstrate that an intrahepatic expression of cytokines in the non parenchymal cells was induced by an LPS challenge but not by a turpentine-induced inflammation. This process could act as a paracrine mechanism in the acute-phase response and play a role in the modulation of hepatic regeneration.