title: Cytokine gene expression in cirrhotic and non-cirrhotic human liver.
abstract: OBJECTIVE
  In order to explore the role of cytokines in the pathogenesis of liver cirrhosis, we analyzed their gene expression in hepatic biopsies from patients with alcoholic liver cirrhosis, post-hepatitis C liver cirrhosis, and with idiopathic portal hypertension without cirrhosis.
  
  
  METHODS
  We assessed the gene expression of interleukins 1 beta, 2, 6, 8, and 10, as well as of tumor necrosis factor-alpha, transforming growth factor-beta and interferon-gamma by a quantitative polymerase chain reaction.
  
  
  RESULTS
  We found high levels of transforming growth factor-beta in post-hepatitis C liver cirrhosis, high to moderate in alcoholic liver cirrhosis and low in non-cirrhotic specimens. Expression of interleukin-10, tumor necrosis factor-alpha, and interferon-gamma genes was detected in most post-hepatitis C liver cirrhosis, but not in idiopathic portal hypertension or alcoholic liver cirrhosis biopsies. The interleukin1-beta, 6 and 8 gene expression was significantly lower in alcoholic liver cirrhosis compared to post-hepatitis C liver cirrhosis, but higher compared to idiopathic portal hypertension specimens. Thus, post-hepatitis C liver cirrhosis samples showed a high degree of cytokine gene expression, whereas in alcoholic liver cirrhosis it tended to be moderate, and restricted to some cytokines (transforming growth factor-beta, interleukin-1, 6 and 8, but not interleukin-10, tumor necrosis factor-alpha or interferon-gamma). In contrast, most non-cirrhotic specimens showed a restricted and low cytokine gene expression.
  
  
  CONCLUSIONS
  These data suggest that transforming growth factor-beta may have an important role in liver fibrosis and inflammation. Interleukin-1 beta, 6, 8, tumor necrosis factor-alpha and interferon-gamma, appear to participate in the pathogenesis of the mild to severe inflammatory phenomena seen in alcoholic and post-hepatitis C liver cirrhosis, respectively. Our data suggest that tumor necrosis factor-alpha does not participate in the hepatocellular damage of alcoholic liver cirrhosis, and indicate that neither interferon-gamma nor interleukin-10, at least at the levels observed in post-hepatitis C liver cirrhosis, are able to counteract the fibrotic/inflammatory process seen in this condition.
authors.affiliation: Department of Immunology and Rheumatology, Instituto Nacional de la Nutrición Salvador Zubirán, México.
authors.forename: L
authors.initials: L
authors.lastname: Llorent
authors.forename: Y
authors.initials: Y
authors.lastname: Richaud-Patin
authors.forename: N
authors.initials: N
authors.lastname: Alcocer-Castillejos
authors.forename: R
authors.initials: R
authors.lastname: Ruiz-Soto
authors.forename: M A
authors.initials: MA
authors.lastname: Mercado
authors.forename: H
authors.initials: H
authors.lastname: Orozco
authors.forename: A
authors.initials: A
authors.lastname: Gamboa-Domínguez
authors.forename: J
authors.initials: J
authors.lastname: Alcocer-Varela
mesh_terms: D000293:Adolescent; D000328:Adult; D000368:Aged; D001706:Biopsy; D016207:Cytokines / Q000235:genetics*; D015870:Gene Expression; D006526:Hepatitis C / Q000150:complications; D006801:Humans; D006975:Hypertension, Portal / Q000378:metabolism* / Q000473:pathology; D008099:Liver / Q000378:metabolism* / Q000473:pathology; D008103:Liver Cirrhosis / Q000378:metabolism* / Q000473:pathology / Q000821:virology; D008104:Liver Cirrhosis, Alcoholic / Q000378:metabolism* / Q000473:pathology; D008875:Middle Aged; D012333:RNA, Messenger / Q000096:biosynthesis
chemical_list: D016207:Cytokines; D012333:RNA, Messenger