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Th1 and Th2 cytokines are elevated in HCV-infected SVR(-) patients treated with interferon-alpha

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Author(s): Wan, L (Wan, Lei); Kung, YJ (Kung, Yung-Jen); Lin, YJ (Lin, Ying-Ju); Liao, CC (Liao, Chiu-Chu); Sheu, JJC (Sheu, Jim J. C.); Tsai, YS (Tsai, Yuhsin); Lai, HC (Lai, Hsueh- Chou); Peng, CY (Peng, Cheng-Yuan); Tsai, FJ (Tsai, Fuu-Jen)

Title: Th1 and Th2 cytokines are elevated in HCV-infected SVR(-) patients treated with interferon-alpha

Source: BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS, 379 (4):

855-860 FEB 20 2009 Language: English Document Type: Article

Author Keywords: HCV; Cytokines; Interferon-alpha; SVR

KeyWords Plus: HEPATITIS-C VIRUS; IMMUNE-RESPONSE; IFN-ALPHA; CELLS;

PROFILE; INTERLEUKIN-8; COMBINATION; CHIMPANZEES; EXPRESSION;

MANAGEMENT

Abstract: Interferon-alpha-based treatment is a standard therapy to cure hepatitis C virus- infected patients. However, the reasons for the failure of interferon-alpha treatment in some patients have not been fully elucidated. We evaluated the differences in the expression levels of various cytokines among patients with and Without Sustained viral response (SVR). We found that the chemokines (MIG and IP-10) and inflammation-related cytokines (IL-6) were transiently elevated in patients with SVR(+) before interferon-alpha treatment and in the early phase of treatment (week 2), indicating that these cytokines may be related to viral clearance.

Furthermore, higher serum levels of Th1 and Th2 cytokines (IL-2, IL-4, IL-5. IL-10, tumor necrosis factor, and IFN-gamma) were observed in SVR(-) than in SVR(+) patients, indicating that they may be associated with ineffective anti-HCV immune response. Our data revealed that the patterns of cytokines varied greatly between SVR(+) and SVR(-) patients before and after IFN-alpha treatment. (C) 2009 Elsevier Inc. All rights reserved.

Addresses: [Lai, Hsueh-Chou; Peng, Cheng-Yuan] China Med Univ Hosp, Div

Hepatogastroenterol, Dept Internal Med, Taichung, Taiwan; [Wan, Lei; Kung, Yung-Jen; Liao, Chiu-Chu; Sheu, Jim J. C.; Tsai, Fuu-Jen] China Med Univ Hosp, Dept Med Genet & Med Res, Taichung, Taiwan; [Wan, Lei; Sheu, Jim J. C.; Tsai, Yuhsin; Tsai, Fuu-Jen] China Med Univ, Grad Inst Chinese Med Sci, Taichung, Taiwan; [Wan, Lei; Lin, Ying-Ju; Tsai, Fuu-Jen]

Asia Univ, Dept Biotechnol, Taichung, Taiwan; [Lin, Ying-Ju] China Med Univ, Grad Inst Acupuncture Sci, Taichung, Taiwan

Reprint Address: Peng, CY, China Med Univ Hosp, Div Hepatogastroenterol, Dept Internal Med, 2 Yuh Der Rd, Taichung, Taiwan.

E-mail Address: [email protected]; [email protected] Funding Acknowledgement:

Funding Agency Grant Number

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National Science Council 94-2320-B-039-042- 95-2320-B-039-045-

China medical University CMU95-061 CMU95-062

We thank Yu-Huei Liang for preparing this manuscript. This study was supported by grants from the National Science Council (94-2320-B-039-042- and 95-2320-B-039-045-), Taipei, Taiwan and grants from China medical University (CMU95-061 and CMU95-062), Taichung, Taiwan.

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BERGQVIST A, 2001, J VIROL, V75, P772.

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BOYER N, 2000, J HEPATOL S1, V32, P98.

BRICE GT, 2001, J IMMUNOL METHODS, V257, P55.

CACCIARELLI TV, 1996, HEPATOLOGY, V24, P6.

CECERE A, 2004, PANMINERVA MED, V46, P171.

COOPER S, 1999, IMMUNITY, V10, P439.

CRIBIER B, 1998, J MED VIROL, V55, P89.

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Cited Reference Count: 32 Times Cited: 0

Publisher: ACADEMIC PRESS INC ELSEVIER SCIENCE

Publisher Address: 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 USA ISSN: 0006-291X

DOI: 10.1016/j.bbrc.2008.12.114

29-char Source Abbrev.: BIOCHEM BIOPHYS RES COMMUN ISO Source Abbrev.: Biochem. Biophys. Res. Commun.

Source Item Page Count: 6

Subject Category: Biochemistry & Molecular Biology; Biophysics ISI Document Delivery No.: 407AT

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