Cytokine Response Associated With Hepatitis C Virus Clearance in Hiv Coinfected Patients Initiating Peg Interferon- Based Therapy.

Nguyen, Truong Tam; Niloofar, Reihani; Rubbo, Pierre-Alain; Nils, Kuster; Bolloré, Karine; Ducos, J; Pageaux, Georges‐Philippe; Reynes, Jacques; Perre, Philippe Van de; Tuaillon, Édouard

doi:10.4084/mjhid.2016.003

Cited by 3 publications

(7 citation statements)

References 51 publications

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“…1 ), suggesting the synergistic effects of poly (I: C) and imiquimod on MoDCs presenting PRRSV antigen. By the way, Th2-type cytokine IL-4 expressed in MoDCs was very low and hard to be detected, so IL-6 and IL-10 were chosen to detect in our study as reported 35 36 .…”

Section: Discussionmentioning

confidence: 99%

“…NF-κB is a transcription factor that regulates the expression of a large number of genes including those involved in inflammation. NF-κB also plays an essential role in innate immune response and many signaling pathways are associated with NF-κB 33 36 37 38 . In previous studies, TRIF mediated innate immune responses in peritoneal mesothelial cells through TLR3 and TLR4 stimulation via activation of NF-κB or MAPKs 39 .…”

Section: Discussionmentioning

confidence: 99%

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Synergy of TLR3 and 7 ligands significantly enhances function of DCs to present inactivated PRRSV antigen through TRIF/MyD88-NF-κB signaling pathway

Chen

et al. 2016

Sci Rep

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PRRS is one of the most important diseases in swine industry. Current PRRS inactivated vaccine provides only a limited protection and cannot induce sufficient cell-mediated immune responses. In this study, we first found that the mRNA and protein levels of Th1-type cytokines (IFN-γ, IL-12) and Th2-type cytokines (IL-6, IL-10) were significantly increased through TRIF/MyD88-NF-κB signaling pathway when porcine peripheral blood monocyte-derived dendritic cells (MoDCs) were treated with poly (I: C) of TLR3 ligand and imiquimod of TLR7 ligand, along with inactivated PRRSV antigen. Meanwhile, the ability of catching PRRSV antigen was also significantly enhanced. In mice experiment, it was found that the PRRSV-specific T lymphocyte proliferation, the percentages of CD4+, CD8+ T lymphocytes and PRRSV-specific CD3+ T cells producing IFN-γ and IL-4, the levels of Th1- and Th2-type cytokines and the titers of neutralization antibody were significantly enhanced in poly (I: C), imiquimod along with inactivated PRRSV group. Taken together, results of our experiments described for the first time that synergy of TLR3 and 7 ligands could significantly enhance the function of DCs to present inactivated PRRSV antigen through TRIF/MyD88-NF-κB signaling pathway and be used as adjuvant candidate for the development of novel PRRS inactivated vaccine.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Synergy of TLR3 and 7 ligands significantly enhances function of DCs to present inactivated PRRSV antigen through TRIF/MyD88-NF-κB signaling pathway

Chen

et al. 2016

Sci Rep

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“…Elucidating the mechanisms underlying IR during the different treatment regimens for HCV is of great importance because the SVR is influenced by the host IR, as previously established by studies on patients undergoing dual therapy 14,17,21,26 . In particular, previous findings indicated that the production of cytokines and chemokines plays an important role in the IR during HCV infection.…”

Section: Discussionmentioning

confidence: 99%

“…Other factors, including the IR, are associated with low SVR rates 10 . Several studies have attempted to further investigate the mechanisms underlying the above findings [11][12][13][14][15] ; however, the results remained ambiguous and controversial.…”

Section: Introductionmentioning

confidence: 99%

“…Several studies showed an association between the abundance of TCD8+ cells and SVR 14,22 , and the quality of the T helper (Th)1 response in the baseline period, and the increase in Th2 cytokines during treatment may define treatment success or failure 11,14,23,24 . These studies were performed on patients treated with dual therapy (IFN alpha or PegIFN and RBV).…”

Section: Introductionmentioning

confidence: 99%

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Influence of the inflammatory response on treatment of hepatitis C with triple therapy

Winckler

Braz

Silva

et al. 2018

Rev. Soc. Bras. Med. Trop.

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Introduction: Chronic hepatitis C is a leading cause of liver disease. Infection triggers an immediate immune response in the host that is mediated by humoral/cellular mechanisms. T cells respond to infection via secretion of cytokines, which inhibit or stimulate one another, leading to cytokine imbalance and ultimately affecting treatment. Studies using interferon (IFN) and ribavirin (RBV) showed that TCD8+ cells and cytokine levels are associated with sustainable virological response (SVR). However, studies that investigated the effects of triple therapy (TT) are limited. Methods: The study included hepatitis C virus (HCV)+ RNA, naives, genotype 1, ≥18 years, and advanced fibrosis (F≥3) patients. Samples were collected at baseline and after 12 weeks (W12) of TT. Six cytokines were analyzed by flow cytometry. Results: Of 31 patients, four were excluded (two deaths, one interrupted TT, and one F2 patient). Of the 27 remaining patients, 21 (78%) were cirrhotic. SVR was achieved in 63% of the patients. The patients had a mean age of 55.11 ± 10.03 years. Analyses at baseline showed that the chemokine CCL5/Regulated on Activation, Normal T Cell Expressed and Secreted (RANTES) (p=0.04) and interleukin (IL)-6 (p=0.02), which was associated with SVR. RANTES (p=0.04) and IL-8 (p=0.01) levels were associated with SVR at W12. Conclusions: Similar to patterns observed during double therapy, IL-6, IL-8, and RANTES levels were associated with SVR in TT, indicating the potential role of interferon in immune response to hepatitis C virus.

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HCV Core Protein Induces Chemokine CCL2 and CXCL10 Expression Through NF-κB Signaling Pathway in Macrophages

et al. 2021

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HCV core protein is the first structural protein synthesized during hepatitis C virus (HCV) infection and replication. It is released from virus infected liver cells and mediates multiple functions to affect host cell response. The innate immune response is the first line of defense against viral infection. After HCV infection, Kupffer cells (KCs) which are liver macrophages play an important role in host innate immune response. Kupffer cells act as phagocytes and release different cytokines and chemokines to counter viral infection and regulate inflammation and fibrosis in liver. Earlier, we have demonstrated that HCV core protein interacts with gC1qR and activates MAPK, NF-κB and PI3K/AKT pathways in macrophages. In this study, we explored the effect of HCV core protein on CCL2 and CXCL10 expression in macrophages and the signaling pathways involved. Upon silencing of gC1qR, we observed a significant decrease expression of CCL2 and CXCL10 in macrophages in the presence of HCV core protein. Inhibiting NF-κB pathway, but not P38, JNK, ERK and AKT pathways greatly reduced the expression of CCL2 and CXCL10. Therefore, our results indicate that interaction of HCV core protein with gC1qR could induce CCL2 and CXCL10 secretion in macrophages via NF-κB signaling pathway. These findings may shed light on the understanding of how leukocytes migrate into the liver and exaggerate host-derived immune responses and may provide novel therapeutic targets in HCV chronic inflammation.

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Cytokine Response Associated With Hepatitis C Virus Clearance in Hiv Coinfected Patients Initiating Peg Interferon- Based Therapy.

Cited by 3 publications

References 51 publications

Synergy of TLR3 and 7 ligands significantly enhances function of DCs to present inactivated PRRSV antigen through TRIF/MyD88-NF-κB signaling pathway

Synergy of TLR3 and 7 ligands significantly enhances function of DCs to present inactivated PRRSV antigen through TRIF/MyD88-NF-κB signaling pathway

Influence of the inflammatory response on treatment of hepatitis C with triple therapy

HCV Core Protein Induces Chemokine CCL2 and CXCL10 Expression Through NF-κB Signaling Pathway in Macrophages

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