2002•PubMedRequires access

The roles of serum IL-18, IL-10, TNF-alpha and sIL-2R in patients with chronic hepatitis C.

Hongyu Jia, Jie Du, Si-he Zhu, MA Yingji, Huanyong Chen, Bao-shan Yang, Huafeng Cai

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Abstract

OBJECTIVE: To identify the roles of serum IL-18, IL-10, TNF-alpha and sIL-2R in the pathogenesis of chronic hepatitis C and the effects of interferon on the mentioned serum cytokines. METHODS: The levels of IL-18, IL-10, TNF-alpha and sIL-2R were detected in 10 healthy controls, 24 asymptomatic HCV carriers, and 27 patients with chronic hepatitis C (before and after IFN treatment) by enzyme linked immunosorbent assay (ELISA). RESULTS: The levels of IL-18, IL-10, TNF-alpha and sIL-2R in the patients of chronic hepatitis C were higher than those in the healthy controls (P<0.05) and in asymptomatic HCV carriers (P<0.05). The values of the mentioned cytokines showed a significant positive correlation to GPT. The levels of the mentioned cytokines decreased obviously after IFN treatment (P<0.05), while the serum levels of IL-10 and sIL-2R reduced in sequence in no-response group, partial-response group and complete-response group. CONCLUSIONS: IL-18, IL-10, TNF-alpha and sIL-2R co-participate in the pathogenesis of chronic hepatitis C, and are used to evaluate the effect of IFN on the immune state of organisms, and IL-10 and sIL-2R are important for predicting the anti-viral efficacy of IFN.

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What this paper is about

OBJECTIVE: To identify the roles of serum IL-18, IL-10, TNF-alpha and sIL-2R in the pathogenesis of chronic hepatitis C and the effects of interferon on the mentioned serum cytokines. METHODS: The levels of IL-18, IL-10, TNF-alpha and sIL-2R were detected in 10 healthy controls, 24 asymptomatic HCV carriers, and 27 patients with chronic hepatitis C (before and after IFN treatment) by enzyme linked immunosorbent assay (ELISA). RESULTS: The levels of IL-18, IL-10, TNF-alpha and sIL-2R in the patients of chronic hepatitis C were higher than those in the healthy controls (P<0.05) and in asymptomatic HCV carriers (P<0.05). The values of the mentioned cytokines showed a significant positive correlation to GPT. The levels of the mentioned cytokines decreased obviously after IFN treatment (P<0.05), while the serum levels of IL-10 and sIL-2R reduced in sequence in no-response group, partial-response group and complete-response group. CONCLUSIONS: IL-18, IL-10, TNF-alpha and sIL-2R co-participate in the pathogenesis of chronic hepatitis C, and are used to evaluate the effect of IFN on the immune state of organisms, and IL-10 and sIL-2R are important for predicting the anti-viral efficacy of IFN.

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Available abstract

OBJECTIVE: To identify the roles of serum IL-18, IL-10, TNF-alpha and sIL-2R in the pathogenesis of chronic hepatitis C and the effects of interferon on the mentioned serum cytokines. METHODS: The levels of IL-18, IL-10, TNF-alpha and sIL-2R were detected in 10 healthy controls, 24 asymptomatic HCV carriers, and 27 patients with chronic hepatitis C (before and after IFN treatment) by enzyme linked immunosorbent assay (ELISA). RESULTS: The levels of IL-18, IL-10, TNF-alpha and sIL-2R in the patients of chronic hepatitis C were higher than those in the healthy controls (P<0.05) and in asymptomatic HCV carriers (P<0.05). The values of the mentioned cytokines showed a significant positive correlation to GPT. The levels of the mentioned cytokines decreased obviously after IFN treatment (P<0.05), while the serum levels of IL-10 and sIL-2R reduced in sequence in no-response group, partial-response group and complete-response group. CONCLUSIONS: IL-18, IL-10, TNF-alpha and sIL-2R co-participate in the pathogenesis of chronic hepatitis C, and are used to evaluate the effect of IFN on the immune state of organisms, and IL-10 and sIL-2R are important for predicting the anti-viral efficacy of IFN.

Key concepts: Medicine, Pathogenesis, Asymptomatic, Alpha interferon, Immunology, Tumor necrosis factor alpha, Immune system, Interferon

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The roles of serum IL-18, IL-10, TNF-alpha and sIL-2R in patients with chronic hepatitis C. — Research Paper | ScholarLens