SERUM TUMOUR NECROSIS FACTOR-α AND TRANSFORMING GROWTH FACTOR-β LEVELS IN CHRONIC HEPATITIS C PATIENTS ARE IMMUNOMODULATED BY THERAPY

Neuman, Manuela G.; Benhamou, Jean‐Pierre; Bourlière, Marc; Ibrahim, Asma; Malkiewicz, Izabella M.; Asselah, Tarik; Martinot–Peignoux, Michelle; Shear, Neil H.; Katz, Gady G.; Akremi, Raoudha; Benali, Souâd; Boyer, Nathalie; Lecomte, Laurence; Breton, Veronique Le; Guludec, Gaelle Le; Marcellin, Patrick

doi:10.1006/cyto.2001.0997

Cited by 51 publications

(42 citation statements)

References 29 publications

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“…A probable although still unclear hypothesis remains their participation in the pathogenesis of infection. According to some authors, in patients with chronic hepatitis C the elevated serum TNF-␣ reflects the intensity of inflammatory lesions (grading) and decreases after anti-viral treatment (Neuman et al 2002). In both groups of our patients, no correlation was observed between grading and cytokine expression, despite higher grading in adults.…”

Section: Discussioncontrasting

confidence: 44%

Expression of Cytokines (TNF-α, IL-1α, and IL-2) in Chronic Hepatitis C: Comparative Hybridocytochemical and Immunocytochemical Study in Children and Adult Patients

Kasprzak

Zabel

Biczysko

et al. 2004

J Histochem Cytochem.

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Section: Discussioncontrasting

confidence: 44%

Expression of Cytokines (TNF-α, IL-1α, and IL-2) in Chronic Hepatitis C: Comparative Hybridocytochemical and Immunocytochemical Study in Children and Adult Patients

Kasprzak

Zabel

Biczysko

et al. 2004

J Histochem Cytochem.

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“…Therefore, we sought to evaluate serum cytokines as noninvasive markers of treatment response. 3,5,[17][18][19] Finally, it is likely that multiple cytokines, particularly endogenous IFNs, are also involved in mediating interactions between HIV and HCV but were not evaluated in the current study. Although a direct comparison between HCV-monoinfected and HCV/HIV-coinfected persons was not considered in the original A5071 study design, the current substudy demonstrates the inability of cytokine levels to predict virologic response to therapy in HCV/HIV-coinfected persons, as has been documented previously in HCV-monoinfected individuals.…”

Section: Discussionmentioning

confidence: 99%

“…4 There is growing evidence that cytokine expression is also linked to HCV treatment response, with lower baseline levels generally correlated with virologic response. [4][5][6][7][8][9][10][11][12][13] Thus, certain cytokines may be useful as easily measured, predictive markers of treatment response.…”

Section: Introductionmentioning

confidence: 99%

Effects of HCV Treatment on Cytokine Expression During HCV/HIV Coinfection

Blackard

Kang

Sherman

et al. 2006

Journal of Interferon & Cytokine Research

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There is growing evidence that cytokine expression is linked to hepatitis C virus (HCV) pathogenesis and treatment response rates among HCV-monoinfected persons. However, because of the profound effects of human immunodeficiency virus (HIV) coinfection on HCV, it is not clear if these observations are also true for HCV/HIV-coinfected individuals. Serum expression of the proinflammatory cytokines interleukin-8 (IL-8) and tumor necrosis factor-α (TNF-α) and the fibrogenic cytokine transforming growth factor-β1 (TGF-β1) were measured in HCV/HIVcoinfected persons at baseline and at week 24 of HCV therapy. Higher levels of IL-8 and TGF-β were demonstrated among nonwhite subjects at baseline. Increases in TNF-α and IL-8 expression were found at week 24 of HCV therapy, suggesting that enhanced proinflammatory cytokine production may occur during HCV treatment. However, cytokine levels were not predictive of HCV virologic, biochemical, or histologic response. Although previous studies conducted among HCV-monoinfected individuals have suggested that cytokine levels could predict the virologic response to therapy, no such associations were observed among HCV/HIV-coinfected persons, suggesting that they may respond differently to treatment than do their HCV-monoinfected counterparts.

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“…TGF-b signaling not only controls cell proliferation, differentiation and apoptosis but also plays an important role in liver repair processes and fibrogenesis through its action on the extracellular matrix. Hepatitis C virus-infected patients have high levels of TGF-b, which correlate with the degree of fibrosis (Nelson et al, 1997;Marcellin et al, 2002;Neuman et al, 2002). On the other hand, wild-type core has been shown to upregulate TGF-b expression at the transcriptional level (Taniguchi et al, 2004) and to induce TGF-b synthesis in hepatic stellate cells, thus promoting fibrogenesis (Bataller et al, 2004).…”

Section: Hepatitis C Virus Proteins and Host-cell Factorsmentioning

confidence: 99%

Viral hepatitis and liver cancer: the case of hepatitis C

2006

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Chronic infection with the hepatitis C virus (HCV) is a major risk factor for the development of hepatocellular carcinoma (HCC) worldwide. The pathogenesis of HCC in HCV infection has extensively been analysed. Hepatitis C virus-induced chronic inflammation and the effects of cytokines in the development of fibrosis and liver cell proliferation are considered as one of the major pathogenic mechanisms. Increasing experimental evidence suggests that HCV contributes to HCC by directly modulating pathways that promote the malignant transformation of hepatocytes. Hepatitis C virus is an RNA virus that does not integrate into the host genome but HCV proteins interact with many host-cell factors well beyond their roles in the viral life cycle and are involved in a wide range of activities, including cell signaling, transcription, cell proliferation, apoptosis, membrane rearrangements, vesicular trafficking and translational regulation. At least four of the HCV gene products, namely HCV core, NS3, NS4B and NS5A, have been shown to exhibit transformation potential in tissue culture and several potentially oncogenic pathways have been shown to be altered by the expression of HCV proteins. Both HCV core and NS5A induce the accumulation of wild-type b-catenin and the Wnt-b-catenin pathway emerges as a common target for HCV (and HBV) in human HCCs, also independently from axin/b-catenin gene mutations. Induction of both endoplasmic reticulum stress and oxidative stress by HCV proteins might also contribute to HCV transformation. Most of the putative transforming functions of the HCV proteins have been defined in artificial cellular systems, which may not be applicable to HCV infection in vivo, and still need to be established in relevant infection and disease models.

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SERUM TUMOUR NECROSIS FACTOR-α AND TRANSFORMING GROWTH FACTOR-β LEVELS IN CHRONIC HEPATITIS C PATIENTS ARE IMMUNOMODULATED BY THERAPY

Cited by 51 publications

References 29 publications

Expression of Cytokines (TNF-α, IL-1α, and IL-2) in Chronic Hepatitis C: Comparative Hybridocytochemical and Immunocytochemical Study in Children and Adult Patients

Expression of Cytokines (TNF-α, IL-1α, and IL-2) in Chronic Hepatitis C: Comparative Hybridocytochemical and Immunocytochemical Study in Children and Adult Patients

Effects of HCV Treatment on Cytokine Expression During HCV/HIV Coinfection

Viral hepatitis and liver cancer: the case of hepatitis C

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