IL-10 plays a central regulatory role in the cytokines induced by hepatitis C virus core protein and polyinosinic acid:polycytodylic acid

Pang, Xiaoli; Wang, Zhaoxia; Zhai, Naicui; Zhang, Qianqian; Song, Haiou; Zhang, Yujiao; Li, Tianyang; Li, Haijun; Su, Lishan; Niu, Junqi; Tu, Zhengkun

doi:10.1016/j.intimp.2016.06.013

Cited by 12 publications

(9 citation statements)

References 42 publications

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“…A study has suggested that chronic hepatitis C patients treated with recombined IL‐10 showed a reduction in fibrosis score, which revealed that IL‐10 is closely associated with the disease progression in CHC patients, and was consistent with our results. As is known, IL‐10 is an important anti‐inflammatory cytokine, IL‐10 may limit hepatic inflammation and injury, but it also contributes to the persistence of HCV virus . Tumor cells also could secret IL‐10 which induced the high serum IL‐10 level in patients with HCC.…”

Section: Discussionmentioning

confidence: 99%

The role of IDO, IL‐10, and TGF‐β in the HCV‐associated chronic hepatitis, liver cirrhosis, and hepatocellular carcinoma

Yang

Gao

Chang

et al. 2018

Journal of Medical Virology

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Indoleamine-2,3-dioxygenase (IDO) is an enzyme that catalyzes tryptophan to kynurenine and studies have revealed that IDO play a vital role in regulation of liver immunity and inflammation activities. This study investigated the association between plasma IDO and disease severity and the possible marker role of IDO in the inflammatory process of hepatitis C. In this study, 80 individuals with HCV infection were retrospectively selected. Plasma levels of IDO, IL-10, and TGF-β were assayed by ELISA. Clinical characteristics of patients, including the levels of ALT, AST, and total bilirubin (TBil) were collected from clinical databases. HCV-related liver cirrhosis (HC-Cirr) and HCV-related Hepatocellular carcinoma (HCV-HCC) had significantly high plasma levels of IDO compared to other patient groups and healthy controls. Plasma IL-10 level were significantly greater in all chronic liver disease groups and with respect to TGF-β, the level was high in all the selected patients with HCV infection compare with controls. Moreover, HCV-HCC patients showed highest values for both IL-10 and TGF-β, with significant difference compared with other groups. In addition, plasma IDO was positively correlated with TGF-β among all patients with HCV infection (r = 0.4509, P < 0.0001), with IL-10 in CHC patients (r = 0.4787, P = 0.0047), with TBil in HCV-Cirr patients (r = 0.4671; P = 0.0093). High level of IDO and TGF-β is associated with hepatocyte necrosis and intrahepatic inflammation, and may be used as an index of disease progression for patients with chronic HCV infection.

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Section: Discussionmentioning

confidence: 99%

The role of IDO, IL‐10, and TGF‐β in the HCV‐associated chronic hepatitis, liver cirrhosis, and hepatocellular carcinoma

Yang

Gao

Chang

et al. 2018

Journal of Medical Virology

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“…Impact of HCV on cytokine production from monocytes: IL-10, an anti-inflammatory cytokine, can be produced by monocytes[ 74 ]. IL-10 has several immunoregulatory functions after HCV infection.…”

Section: Impact Of Hcv On the Mpsmentioning

confidence: 99%

“…In our lab, we studied the network of cytokines that regulate IL-10 production and the cytokines regulated by IL-10 upon HCV infection[ 74 ]. The stimulation of monocytes with HCVc and polyI:C induces the secretion of TNF-α, IL-1β, IL-10, and type I IFN.…”

Section: Impact Of Hcv On the Mpsmentioning

confidence: 99%

“…The stimulation of monocytes with HCVc and polyI:C induces the secretion of TNF-α, IL-1β, IL-10, and type I IFN. Interestingly, TNF-α, IL-1β, and IFN promote the IL-10 production, whereas high IL-10 levels inhibit TNF-α, IL-1β, and IFN production[ 74 ]. Furthermore, receptors for IL-10 on monocytes are also elevated during HCV infection and the type I as well as type III IFNs upregulate the IL-10 monocyte receptors, leading to higher sensitivity of monocytes to IL-10[ 83 ].…”

Section: Impact Of Hcv On the Mpsmentioning

confidence: 99%

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Mononuclear phagocyte system in hepatitis C virus infection

Liu

et al. 2018

WJG

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The mononuclear phagocyte system (MPS), which consists of monocytes, dendritic cells (DCs), and macrophages, plays a vital role in the innate immune defense against pathogens. Hepatitis C virus (HCV) is efficient in evading the host immunity, thereby facilitating its development into chronic infection. Chronic HCV infection is the leading cause of end-stage liver diseases, liver cirrhosis, and hepatocellular carcinoma. Acquired immune response was regarded as the key factor to eradicate HCV. However, innate immunity can regulate the acquired immune response. Innate immunity-derived cytokines shape the adaptive immunity by regulating T-cell differentiation, which determines the outcome of acute HCV infection. Inhibition of HCV-specific T-cell responses is one of the most important strategies for immune system evasion. It is meaningful to illustrate the role of innate immune response in HCV infection. With the MPS being the important factor in innate immunity, therefore, understanding the role of the MPS in HCV infection will shed light on the pathophysiology of chronic HCV infection. In this review, we outline the impact of HCV infection on the MPS and cytokine production. We discuss how HCV is detected by the MPS and describe the function and impairment of MPS components in HCV infection.

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“…In chronic HCV infection, the functionality of both innate and adaptive immunity is affected. Monocytes are bone marrow-derived phagocytes involved in critical immune processes that convert innate immunity to adaptive to defend the host against pathogens (4,5). Our previous research study demonstrated that HCV inhibits IL-12 production and STAT-1 phosphorylation (p-STAT-1) in monocyte (M) through crosstalk between Tim-3 and PD-1 and SOCS-1 (6).…”

Section: Introductionmentioning

confidence: 99%

miR-155 regulates pro- and anti-inflammatory cytokine expression in human monocytes during chronic hepatitis C virus infection

Zhou¹,

Zhang²,

Zheng³

et al. 2021

Ann Transl Med

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Background: Hepatitis C virus (HCV) dysregulates innate and adaptive immune responses while monocytes (M) play a crucial role in linking innate and adaptive immunity to control viral infection. A transcription factor T-bet is upregulated to dampen M functions via the c-Jun N-terminal kinase (JNK) pathway, followed by enhanced Tim-3 expression in chronic HCV infection. However, the molecular mechanisms that control the expression in M are yet unknown. miR-155 has been implicated as a key regulator controlling diverse biological processes through posttranscriptional repression, but the influences of miR-155 on these regulators and effectors still need to be studied. Methods: Forty HCV-infected patients and 40 healthy subjects (HS) were recruited, THP-1 cells (human acute monocyte leukemia cell line) were cultured with HCV-infected Huh 7.5 cells. The expression levels of miR-155 and JNK1/JNK2/JNK3 were measured by real-time RT-PCR. IL-10/IL-12 was detected by flow cytometry. THP-1 cells were transfected with mimics-155 and negative control, SOCS1, p-STAT1, p65, p-smad, p-p38, and p-JNK were measured by Western blot. TNF-α levels were measured by ELISA. Student's t-test was used in statistics. Results: The study showed that miR-155 was upregulated in CD14 + M in HCV-infected patients compared to healthy subjects (P<0.05). Moreover, the upregulation of miR-155 in CD14 + M from HCV-infected patients induced TNF-α production and JNK gene expression, which, in turn, led to T-bet upregulation. Also, miR-155 upregulation in CD14 + M of HCV-infected patients increased the IL-12 and decreased the IL-10 production. Conclusions: The obtained results indicated that miR-155 upregulation in M during HCV infection enhances the activation of TNF-α and JNK pathways, promotes the expression of transcription factor T-bet, and triggers pro-and anti-inflammatory mediators. Together, these data reveal new information regarding the mechanisms of chronic HCV infection.

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IL-10 plays a central regulatory role in the cytokines induced by hepatitis C virus core protein and polyinosinic acid:polycytodylic acid

Cited by 12 publications

References 42 publications

The role of IDO, IL‐10, and TGF‐β in the HCV‐associated chronic hepatitis, liver cirrhosis, and hepatocellular carcinoma

The role of IDO, IL‐10, and TGF‐β in the HCV‐associated chronic hepatitis, liver cirrhosis, and hepatocellular carcinoma

Mononuclear phagocyte system in hepatitis C virus infection

miR-155 regulates pro- and anti-inflammatory cytokine expression in human monocytes during chronic hepatitis C virus infection

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