title: Expression of interleukin-17 associated with disease progression and liver fibrosis with hepatitis B virus infection: IL-17 in HBV infection.
abstract: OBJECTIVE
  As a proinflammatory cytokine, interleukin-17 (IL-17) contributes to the inflammation of many autoimmune diseases. We examined IL-17 levels in serum and tissues from patients with chronic hepatitis B virus infection (HBV), and especially evaluated the role of IL-17 in the pathogenesis and progression of liver fibrosis.
  
  
  METHODS
  Whole venous blood was obtained from four patient groups: chronic hepatitis B (CHB, n = 47), liver cirrhosis (LC, n = 49), primary hepatocellular carcinoma (PHC, n = 44), chronic liver failure (CLF, n = 33), and a normal control group (n = 20). HBsAg was positive in all patients. Liver biopsy samples were acquired from asymptomatic HBsAg carriers (ASC, n = 35), CHB (n = 57), and LC (n = 31) patients. We performed ELISA to measure IL-17 levels in serum samples, and used reverse RT-PCR to measure IL-17 mRNA levels in peripheral blood mononuclear cells (PBMC). IL-17 protein expression was detected in liver biopsy tissues by immunohistochemistry.
  
  
  RESULTS
  Compared to normal controls, serum IL-17 protein and mRNA levels were significantly higher in the four infection groups. LC patients exhibited the highest serum IL-17 and PBMC mRNA levels. No significant differences were found between the other three groups. High levels of IL-17 were also observed in tissues from CHB and LC patients, compared to ASC. IL-17 expression was mainly located in the portal area and was positively correlated with inflammation grade and fibrosis stage.
  
  
  CONCLUSIONS
  IL-17 expression was found to be increased with increasing degrees of liver fibrosis. This suggests that IL-17 may not only induce the inflammation, but also contribute to disease progression and chronicity.
  The virtual slide(s) for this article can be found here: http://www.diagnosticpathology.diagnomx.eu/vs/5306959258322482.
authors: Shandong University, School of Medicine, Jinan, China. crbdwj@126.com
authors: Wen-Jun
authors: WJ
authors: Du
authors: Jun-Hui
authors: JH
authors: Zhen
authors: Zhao-Qing
authors: ZQ
authors: Zeng
authors: Zhao-Min
authors: ZM
authors: Zheng
authors: Yan
authors: Y
authors: Xu
authors: Lai-Ying
authors: LY
authors: Qin
authors: Shi-Jun
authors: SJ
authors: Chen
mesh_terms: D000328:Adult; D015415:Biomarkers / Q000097:blood; D001706:Biopsy; D006528:Carcinoma, Hepatocellular / Q000276:immunology / Q000473:pathology / Q000821:virology; D016022:Case-Control Studies; D018450:Disease Progression; D058625:End Stage Liver Disease / Q000276:immunology / Q000473:pathology / Q000821:virology; D004797:Enzyme-Linked Immunosorbent Assay; D005260:Female; D006514:Hepatitis B Surface Antigens / Q000097:blood; D019694:Hepatitis B, Chronic / Q000097:blood / Q000150:complications / Q000235:genetics / Q000276:immunology* / Q000473:pathology; D006801:Humans; D007150:Immunohistochemistry; D018836:Inflammation Mediators / Q000097:blood*; D020381:Interleukin-17 / Q000032:analysis* / Q000097:blood / Q000235:genetics; D007963:Leukocytes, Mononuclear / Q000276:immunology*; D008099:Liver / Q000276:immunology* / Q000473:pathology / Q000821:virology; D008103:Liver Cirrhosis / Q000097:blood / Q000235:genetics / Q000276:immunology* / Q000473:pathology / Q000821:virology; D008113:Liver Neoplasms / Q000276:immunology / Q000473:pathology / Q000821:virology; D008297:Male; D008875:Middle Aged; D011379:Prognosis; D012333:RNA, Messenger / Q000097:blood; D060888:Real-Time Polymerase Chain Reaction; D020133:Reverse Transcriptase Polymerase Chain Reaction; D015854:Up-Regulation; D055815:Young Adult
chemical_list: D015415:Biomarkers; D006514:Hepatitis B Surface Antigens; D018836:Inflammation Mediators; D020381:Interleukin-17; D012333:RNA, Messenger