RANTES, TNF-α, Oxidative Stress, and Hematological Abnormalities in Hepatitis C Virus Infection

Tawadrous, Gamil A.; Aziz, Ahmed Abdel; Amin, Dalia Gamil; Eldemery, Ahmed; Mostafa, Mostafa Abdel-Aziz

doi:10.2310/jim.0b013e318254519e

Cited by 22 publications

(11 citation statements)

References 39 publications

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“…Earlier study reported that infections are likely associated with oxidative stress in a number of ways. 13 In our study we found the severity of oxidative stress was more prominent among the CF-VAD patients with infection indicating the active involvement of oxidative stress in this process.…”

Section: Discussionsupporting

confidence: 52%

Infection, Oxidative Stress, and Changes in Circulating Regulatory T Cells of Heart Failure Patients Supported by Continuous-Flow Ventricular Assist Devices

Mondal

Sobieski

Pham³

et al. 2017

ASAIO Journal

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The objective of this study was to investigate the changes in oxidative stress (OS) and circulating regulatory T cells (Tregs) of the immune system in CF-VAD patients with or without infection. We recruited 16 CF-VAD patients (5 with infection and 11 without infection) and 7 healthy volunteers. Generation of reactive oxygen species (ROS) from lymphocytes, superoxide dismutase (SOD) in erythrocyte, total antioxidant capacity (TAC) and oxidized low density lipoprotein (oxLDL) in plasma were measured. Circulating Tregs were evaluated by flow cytometry. HF patients had elevated OS than healthy volunteers as evident from higher lymphocyte ROS, elevated oxLDL as well as depleted SOD and TAC levels. At baseline, HF patients had decreased % of Tregs (5.12±1.5 vs. 8.14±3.01%, p<0.01) when compared to healthy volunteers. Post-implant patients with infection illustrated 35% and 44% rise in ROS and oxLDL respectively, 31% decrease in TAC and marked rise in % of Tregs (14.27±3.17 vs.9.38± 3.41%, p<0.01) when compared to the patients without infection. Elevated OS and rise in Tregs were more prominent in CF-VAD patients with infection. In conclusion, OS and compromised immune system may be important indicators of systemic response of the body to CF-VAD among HF patients with infection.

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Section: Discussionsupporting

confidence: 52%

Infection, Oxidative Stress, and Changes in Circulating Regulatory T Cells of Heart Failure Patients Supported by Continuous-Flow Ventricular Assist Devices

Mondal

Sobieski

Pham³

et al. 2017

ASAIO Journal

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“…Concentration of chemokine Rantes is higher in HBV infected patients than in the controls [18]. Besides, significant increases of the levels of Rantes, TNF-a, and NO in Hepatitis C virus-infected patients are observed [19]. Another study has shown that MCP-1 plasma levels are higher in both alcoholic liver disease and alcoholic hepatitis patients than in the controls, and alcoholic hepatitis patients have significantly higher hepatic expression of MCP-1 [20].…”

Section: Discussionmentioning

confidence: 82%

EGCG attenuates pro-inflammatory cytokines and chemokines production in LPS-stimulated L02 hepatocyte

Liu

Qian

Chen

et al. 2014

ABBS

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Endotoxin lipopolysaccharide (LPS) plays an important role in the acceleration of inflammatory reaction of hepatitis as the second attack. Compounds that can prevent inflammation by targeting LPS have potential therapeutic clinical application. Epigallocatechin-3-gallate (EGCG) has potent hepatocyte-protective effect and mild anti-hepatitis virus function. Here, we investigated whether EGCG attenuated the severity of inflammatory response in LPS-stimulated L02 hepatocytes. L02 hepatocytes were pretreated with EGCG for 2 h, then stimulated by LPS at 250 ng/ml. The expression levels of chemokine regulated upon activation normal T-cell expressed and secreted (Rantes) and monocyte chemotactic protein-1 (MCP-1), pro-inflammatory cytokines tumor necrosis factor-a (TNF-a) and interferon-g, adhesion molecule intercellular adhesion molecule-1 (ICAM-1), oxidant stress molecules nitric oxide (NO), vascular endothelial growth factor (VEGF), and matrix metalloproteinase-2 (MMP-2) were tested by enzyme-linked immunosorbent assay. The expression of total extracellular signal-regulated kinase 1/2 (ERK1/2), phospho-ERK1/2 (p-ERK1/2), p-AKT, total p38, phospho-p38 (p-p38), total p65 and phospho-p65 (p-p65), IkBa, phospho-IkBa (p-IkBa) and TNF receptor associated factor 2 were tested by western blot analysis. Our results showed that pre-treatment with EGCG could significantly reduce the production of TNF-a, Rantes, MCP-1, ICAM-1, NO, VEGF, and MMP-2 in LPS-stimulated L02 hepatocytes in a dose-dependent manner. The effect of EGCG may be related to the inhibition of nuclear factor-kB (NF-kB) and mitogen-activated protein kinase (MAPK) signaling pathways by down-regulation of p-IkBa, p65, p-p65, p-p38, p-ERK1/2, and p-AKT. These results indicate that EGCG suppresses LPS-induced inflammatory response and oxidant stress and exerts its hepatocyte-protective activity partially by inhibiting NF-kB and MAPK pathways.

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“…Chronic HCV infection is associated with production of the pro-inflammatory cytokine TNFα in vivo [46], [47]. Furthermore, TNFα is an important regulatory factor in HIV pathogenesis and acts through NF-kB to activate HIV transcription [18], [56].…”

Section: Resultsmentioning

confidence: 99%

“…HCV also has several immunoregulatory effects on the host that influence pathogenicity and may facilitate interactions with the HIV promoter. For example, tumor necrosis factor alpha (TNFα), a monocyte/macrophage-derived pro-inflammatory cytokine, is elevated during chronic HCV infection but also plays a pivotal role in HIV pathogenesis by inducing viral transcription via the NF-kB pathway [18], [45]–[47].…”

Section: Introductionmentioning

confidence: 99%

Effects of HCV on Basal and Tat-Induced HIV LTR Activation

et al. 2013

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Hepatitis C virus (HCV) co-infection occurs in ∼30–40% of the HIV-infected population in the US. While a significant body of research suggests an adverse effect of HIV on HCV replication and disease progression, the impact of HCV on HIV infection has not been well studied. Increasing data suggest that hepatocytes and other liver cell populations can serve as reservoirs for HIV replication. Therefore, to gain insight into the impact of HCV on HIV, the effects of the HCV Core protein and infectious hepatitis C virions were evaluated on basal and Tat-induced activation of the HIV long terminal repeat (LTR) in hepatocytes. The HIV LTR was highly induced by the HIV transactivator protein Tat in hepatocytes. Activation varied according to the number of NF-kB binding sites present in the LTRs from different HIV subtypes. Involvement of the NF-kB binding pathway in LTR activation was demonstrated using an NF-kB inhibitor and deletion of the NF-kB binding sites. TNFα, a pro-inflammatory cytokine that plays an important role in HIV pathogenesis, also induced LTR activity in hepatocytes. However, HIV LTR activity was suppressed in hepatocytes in the presence of HCV Core protein, and the suppressive effect persisted in the presence of TNFα. In contrast, infectious hepatitis C virions upregulated HIV LTR activation and gene transcription. Core-mediated suppression remained unaltered in the presence of HCV NS3/4A protein, suggesting the involvement of other viral/cellular factors. These findings have significant clinical implications as they imply that HCV could accelerate HIV disease progression in HIV/HCV co-infected patients. Such analyses are important to elucidate the mechanisms by which these viruses interact and could facilitate the development of more effective therapies to treat HIV/HCV co-infection.

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RANTES, TNF-α, Oxidative Stress, and Hematological Abnormalities in Hepatitis C Virus Infection

Abstract: The data support the concept of chemokines (RANTES) as mediators of liver cell injury in HCV infection. In addition, MDA and NO levels might be used as monitoring markers for oxidative stress in hepatitis C infection.

Cited by 22 publications

References 39 publications

Infection, Oxidative Stress, and Changes in Circulating Regulatory T Cells of Heart Failure Patients Supported by Continuous-Flow Ventricular Assist Devices

Infection, Oxidative Stress, and Changes in Circulating Regulatory T Cells of Heart Failure Patients Supported by Continuous-Flow Ventricular Assist Devices

EGCG attenuates pro-inflammatory cytokines and chemokines production in LPS-stimulated L02 hepatocyte

Effects of HCV on Basal and Tat-Induced HIV LTR Activation

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