Cytokines as predictors for sustained response and as markers for immunomodulation in patients with chronic hepatitis C

Neuman, Manuela G.; Benhamou, Jean‐Pierre; Malkiewicz, Izabella M.; Akremi, Raoudha; Shear, Neil H.; Asselah, Tarik; Ibrahim, Asma; Boyer, Nathalie; Martinot–Peignoux, Michelle; Jacobson-Brown, Pearl; Katz, Gady G.; Breton, Veronique Le; Guludec, Gaelle Le; Suneja, Ashima; Marcellin, Patrick

doi:10.1016/s0009-9120(01)00212-0

Cited by 64 publications

(61 citation statements)

References 26 publications

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“…Therefore, we proposed TNF-α as a marker of sustained response for the HCV population undergoing standard therapy. These results are in line with other studies as Neuman et al who reported that serum TNF-α levels are significantly higher among patients with CHC compared to healthy volunteers (30). Also, Fallahi et al stated that production of inappropriate levels of IL-6 and tumor necrosis factor-alpha (TNF-α) has been associated with the progression of chronic hepatitis C (31).…”

Section: Discussionsupporting

confidence: 89%

Adhesive molecules and inflammatory markers among hepatitis C virus Saudi patients

Al-Jiffri

2017

Electron J Gen Med

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Background:Currently, about 2% of population are affected with hepatitis C worldwide, chronic hepatitis C (CHC) is the major cause of hepatic cirrhosis and referral for liver transplant. However, there is a high need for noninvasive methods for assessment of hepatocellular damage. Objective: The purpose of this study was to determine the strength of the association between adhesive molecules and inflammatory markers among hepatitis C virus Saudi patients. Methods: One hundred patients with chronic hepatitis C virus infection(64 males and 36 females, their age ranged from 28 to 53 years with circulating anti-HCV antibodies were equally categorized into two study groups: patients with CHC and patients with liver cirrhosis (LC). Also, one fifty healthy subjects were included as healthy controls. Serum alanine aminotransferase (ALT), soluble intercellular adhesion molecule1 (sICAM-1); Soluble vascular adhesion molecule 1(sVCAM-1); Soluble E-selectin(s-E-selectin) and Tumor necrosis factor-alpha (TNF-α) were assayed for all participants. Results: We observed elevation with regard to the healthy controls group in the parameters of ALT, sICAM-1, sVCAM-1, s-E-selectin and TNF-α for patients with CHC and patients with liver cirrhosis (LC). Also, a significant positive correlation between serum TNF-α, sICAM-1, sVCAM-1 and ALT values was detected. Conclusion:In conclusion, our results confirm that, in patients with chronic virus hepatitis and liver cirrhosis there is a significant positive correlation between serum TNF-α, sICAM-1, sVCAM-1 and ALT values. These findings suggest that serum TNF-α levels could be used as a sensitive predictor of liver inflammation, while serum ICAM-1 can be considered as a marker of hepatic necrosis and inflammatory activity in chronic hepatitis, while serum VCAM-1 is an indicator for the severity of liver cirrhosis.

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Section: Discussionsupporting

confidence: 89%

Adhesive molecules and inflammatory markers among hepatitis C virus Saudi patients

Al-Jiffri

2017

Electron J Gen Med

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“…12,13,15,16 These data suggest that serum levels of cytokines, such as IL-8, TNF-α, and TGF-β1, might be important predictors of the virologic response to HCV therapy. In the present analysis, we measured cytokine levels to determine if cytokine expression was also associated with HCV virologic, histologic, or biochemical response among HCV/HIV-coinfected persons.…”

Section: Discussionmentioning

confidence: 91%

“…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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“…122,127 Marked upregulation of TLR2 and TLR4 was reported in patients with chronic HCV infection irrespective of HCV genotype and viral load 128 and was detected in hepatocytes, Kupffer cells, and peripheral blood monocytes. 129 TLR2-and TLR4-induced TNF␣ production and circulating TNF␣ levels are increased in HCV-infected patients 127,130 while HCV replication, unlike other RNA viruses, is resistant to TNF␣. 131 Thus, TLR2-mediated activation by HCV proteins may contribute to the increased pro-inflammatory cytokine activation and hepatocyte damage in chronic HCV infection.…”

Section: Prrs In Liver Diseasesmentioning

confidence: 99%

“…131 Thus, TLR2-mediated activation by HCV proteins may contribute to the increased pro-inflammatory cytokine activation and hepatocyte damage in chronic HCV infection. 130,132 Of the other viruses that cause hepatitis, members of the herpes virus family were shown to activate TLRs. 133 Human cytomegalovirus activates inflammatory cytokine responses via CD14 and Toll-like receptor 2, 134 while HSV activates via TLR9, 135 suggesting that TLR-induced signals may play a role in virus-induced liver damage.…”

Section: Prrs In Liver Diseasesmentioning

confidence: 99%