Abstract
Background/objectivesAs 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.Materials and methodsWhole 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.ResultsCompared 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.ConclusionsIL-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.Virtual SlidesThe virtual slide(s) for this article can be found here: http://www.diagnosticpathology.diagnomx.eu/vs/5306959258322482
Highlights
Hepatitis B is a major cause of liver diseases causing chronic hepatitis B virus (HBV) infection in an estimated 400 million people worldwide [1]
A recent study indicates that anomalous induction of IL-17-expressing CD8+ T cells lacking the transcription factor, T-bet, and eomesodermin was found to be associated with a progressive inflammatory and wasting syndrome characterized by multi-organ infiltration of neutrophils during infection by lymphocytic choriomeningitis virus (LCMV) [21]
There were no significant differences between serum IL-17 levels in patients with primary hepatic carcinoma (PHC) compared to the ones with Chronic hepatitis B (CHB) (P = 0.029), between the patients with CHB or the ones with chronic severe hepatitis (P = 0.260), and between the patients with the chronic severe hepatitis or ones with PHC (P = 0.435) (Table 1)
Summary
Hepatitis B is a major cause of liver diseases causing chronic hepatitis B virus (HBV) infection in an estimated 400 million people worldwide [1]. Tcell-mediated adaptive immune response plays an essential role in chronic HBV infection. T cell-mediated adaptive immunity imposes a “double-edged sword” by reducing levels of HBV at the expense of organ injury. The IL-17 family of cytokines has been reported to be involved in many immune processes, most notably in inducing and mediating proinflammatory responses. This proinflammatory activity is exemplified by their involvement in pulmonary inflammatory responses.Th17 cells are distinct from Th1 or Th2 cells [8]. Differentiation of mouse Th17 cells is dependent on transforming growth factor-β (TGF-β) and interleukin-6 (IL-6) [9,10,11]. IL-17 may play an immunopathological role, resulting in tissue damage during viral infection
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