Significance of correlation between interferon-γ and soluble intercellular adhesion molecule-1 and interleukin-17 in hepatitis B virus-related cirrhosis.

Clin Res Hepatol Gastroenterol

Division of Gastroenterology and Hepatology, Digestive Disease Institute, Tongji Hospital, Tongji University School of Medicine, Shanghai 200065, PR China.

Published: December 2013

Background And Objective: Hepatitis B virus (HBV)-related cirrhosis is known to be associated with chronic hepatic inflammation. The present study aimed to examine the correlation between inflammatory mediators INF-γ, IL-17, and sICAM-1 in HBV cirrhotic patients.

Methods: The levels of sICAM-1, interleukin-17, and IFN-γ were measured with enzyme-linked immunosorbent assays in 120 cirrhotic patients with HBV and 270 sex- and age-matched healthy controls. Total bilirubin (TB) was measured and the association between TB and IFN-γ, sICAM-1, interleukin-17 were analyzed. The levels of these cytokines in serum and the association between IFN-γ and sICAM-1 as well as interleukin-17 were investigated. Relationships between these cytokines and Child-Pugh classes were analyzed in patients.

Results: Age and sex were similar, but TB values were significantly different between the two groups (P<0.001). Serum levels of sICAM-1, interleukin-17, and IFN-γ were significantly higher in cirrhotic patients with HBV than in controls (P<0.001 for both). TB levels were positively correlated with IFN-γ, interleukin-17 and sICAM-1 levels. Significantly positive correlations were also found between IFN-γ and interleukin-17 as well as sICAM-1 (r=0.817 and r=0.561, respectively, P<0.01). There were significant differences between the studied cytokines (sICAM-1, interleukin-17, and IFN-γ) and Child-Pugh classes (P<0.01).

Conclusions: The increased IFN-γ level was correlated with both IL-17 and sICAM-1, and it may primarily play a role as cytokines trigger in liver injury. Both IL-17 and sICAM-1 may synergistically contribute to liver damage.

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http://dx.doi.org/10.1016/j.clinre.2013.05.010DOI Listing

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