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Proapoptotic IL-18 in patients with chronic hepatitis C treated with pegylated interferon-alpha

He YingLi1, Lin Shumei, Yang Qian

  • 1Infectious Diseases Department, The First Affiliated Hospital of Xi'an Jiaotong University, Xi'an 710061, Shaanxi Province, China.

Clinical and Experimental Medicine
|February 25, 2009
PubMed

Insights

Hepatitis C virus (HCV) infection involves elevated Interleukin-18 (IL-18) levels, which decrease with successful pegylated interferon (PEG-IFN) alpha treatment. Persistent high IL-18 indicates treatment failure and ongoing liver inflammation.

Area of Science:

  • Hepatology
  • Immunology
  • Virology

Background:

  • Hepatitis C virus (HCV) infection is a significant global health issue causing chronic liver disease.
  • HCV is not directly cytopathic; immune responses, particularly cytokine-mediated, are crucial in its pathogenesis.
  • Interleukin-18 (IL-18), a cytokine produced by monocytes/macrophages, enhances T cell responses and promotes Th1 immunity.

Purpose of the Study:

  • To investigate the sequential changes in IL-18 levels during pegylated interferon (PEG-IFN) alpha treatment in Hepatitis C patients.
  • To establish the correlation between plasma IL-18 levels and alanine aminotransferase (ALT) in chronic hepatitis C.
  • To determine if IL-18 levels can predict treatment response to PEG-IFN alpha therapy.

Main Methods:

  • Longitudinal study of 48 weeks involving patients with chronic hepatitis C undergoing PEG-IFN alpha-2a treatment.
  • Measurement of plasma IL-18 levels at baseline and follow-up time points (week 24 and week 48).
  • Correlation analysis between IL-18 levels, ALT, and treatment outcomes (viral clearance and hepatic inflammation).

Main Results:

  • HCV-infected patients exhibited significantly higher IL-18 levels compared to healthy donors.
  • Plasma IL-18 levels strongly correlated with alanine aminotransferase (ALT) levels (r = 0.77, P < 0.05), indicating association with hepatic inflammation.
  • Successful PEG-IFN alpha-2a treatment led to a marked decline in IL-18 levels and remission of liver inflammation in responders.
  • Non-responders showed persistent elevated IL-18 levels, suggesting a link to treatment failure.

Conclusions:

  • Elevated IL-18 levels are associated with active HCV infection and hepatic inflammation.
  • Declining IL-18 levels during PEG-IFN therapy indicate successful viral clearance and treatment response.
  • Persistent high IL-18 levels during therapy are indicative of PEG-IFN treatment failure in chronic hepatitis C.

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