Monocyte chemoattractant protein 1 released from macrophages induced by hepatitis C virus promotes monocytes migration

Liu, Yuan; Wang, Wenbo; Zou, Ziying; Fan, Quanshui; Hu, Zonghai; Feng, Ziliang; Zhu, Bing; Xiong, Jie

doi:10.1016/j.virusres.2017.08.013

Cited by 13 publications

(9 citation statements)

References 33 publications

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“…Our study also confirms that the production of inflammatory cytokines and chemokines is enhanced in patients with chronic HCV infection and is downregulated by viral eradication . Indeed, antiviral therapy significantly improved IL1‐ra, IL2, IL5, FGF‐basic, GM‐CSF, IFN‐gamma, CCL2, CCL3, CCL4, CCL11, CXCL10, PDGF‐BB, and TNF‐alpha plasma levels.…”

Section: Discussionsupporting

confidence: 83%

“…Indeed, this result may be affected by the relatively short follow-up period, as the evaluation of these parameters was performed 1 year after the end of the DAA treatment, and also by the fact that only patients with well-compen- Our study also confirms that the production of inflammatory cytokines and chemokines is enhanced in patients with chronic HCV infection and is downregulated by viral eradication. [28][29][30][31][32][33][34][35][36][37] Indeed, antiviral therapy significantly improved IL1-ra, IL2, IL5, FGF-basic, , faecal calprotectin) before and 1 y after the end of direct-acting antiviral (DAA) treatment. IL: interleukin; ra:receptor agonist; FGF: fibroblast growth factor; G-CSF: granulocyte colony-stimulating factor; GM-CSF: granulocytemacrophage colony-stimulating factor; IFN: interferon; CCL: C-C motif chemokine ligand; CXCL: C-X-C motif chemokine ligand; PDGF: plateletderived growth factor; TNF: tumour necrosis factor GM-CSF, IFN-gamma, CCL2, CCL3, CCL4, CCL11, CXCL10, PDGF-BB, and TNF-alpha plasma levels.…”

Section: P-value (Hcv Post-daa Vs Controls)mentioning

confidence: 99%

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Influence of hepatitis C virus eradication with direct‐acting antivirals on the gut microbiota in patients with cirrhosis

Ponziani

Putignani

Sterbini

et al. 2018

Aliment Pharmacol Ther

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Summary Background The cure of hepatitis C virus (HCV) infection may contribute to the reduction of liver fibrosis progression and potentially influence the gut‐liver axis. Aim To investigate the influence of HCV infection eradication with direct‐acting antivirals (DAAs) on the gut microbiota composition as well as on intestinal and systemic inflammatory parameters in patients with cirrhosis. Methods Consecutive patients with HCV‐related cirrhosis receiving DAA treatment were included. The gut microbiota composition, intestinal permeability, and inflammation were assessed before treatment and after 1 year. Clinical outcomes such as episodes of decompensation and markers of liver fibrosis were evaluated over a 2‐year follow‐up period. Results The gut microbiota alpha diversity in cirrhotic patients, which was lower than that in healthy subjects, was significantly improved by the cure of HCV infection and a shift in the overall gut microbiota composition was observed compared to baseline. The abundance of potentially pathogenic bacteria (Enterobacteriaceae, Enterococcus, and Staphylococcus) was decreased after treatment. The gut microbiota composition was associated with the inflammatory profile and markers of liver fibrosis. Although a significant reduction in the serum levels of cytokines and chemokines was observed post‐DAA treatment, measures of intestinal permeability and inflammation remained unchanged. Conclusions Cure of HCV infection with DAAs in patients with cirrhosis is associated with a modification of the gut microbiota, which correlates with fibrosis and inflammation but does not improve intestinal barrier function.

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Section: Discussionsupporting

confidence: 83%

Section: P-value (Hcv Post-daa Vs Controls)mentioning

confidence: 99%

Influence of hepatitis C virus eradication with direct‐acting antivirals on the gut microbiota in patients with cirrhosis

Ponziani

Putignani

Sterbini

et al. 2018

Aliment Pharmacol Ther

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“…Monocyte chemoattractant protein 1 (MCP1), also known as C‐C motif chemokine ligand 2 (CCL2), is an initiating cytokine of the inflammatory cascade secreted by endothelial cells, monocytes and other cells . MCP1 affects monocyte migration together with subsequent macrophage polarization and recruitment of immune cells to the site of injury . An increasing number of evidence have shown that in animal models of sepsis, the high levels of MCP1 are strongly correlated with organ dysfunction and mortality …”

Section: Introductionmentioning

confidence: 99%

“…14 MCP1 affects monocyte migration together with subsequent macrophage polarization and recruitment of immune cells to the site of injury. 15,16 An increasing number of evidence have shown that in animal models of sepsis, the high levels of MCP1 are strongly correlated with organ dysfunction and mortality. 17 An important characteristic of sepsis is endothelial activation.…”

mentioning

confidence: 99%

Plasma PTX3, MCP1 and Ang2 are early biomarkers to evaluate the severity of sepsis and septic shock

et al. 2019

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Sepsis is associated with significant mortality. Early diagnosis and prognosis of patients with sepsis is still a difficult clinical challenge. In this study, the ability of plasma PTX3 (pentraxin 3), MCP1 (monocyte chemoattractant protein 1) and Ang (angiopoietin)1/2 was investigated to evaluate the severity of sepsis. Blood samples were obtained from 43 patients with sepsis. A total of 33 post‐surgery patients with infections and 25 healthy individuals served as controls. The results showed that plasma PTX3, MCP1 and Ang2 significantly increased in patients on the first day of septic shock onset, while sepsis patients had significantly higher Ang2 level, compared with controls. Furthermore, PTX3, MCP1 and Ang2 had high AUROC values in patients with septic shock on the first day of sepsis onset. The findings suggest that PTX3, MCP1 and Ang2 maybe early predictors to evaluate the severity of sepsis and septic shock with the latest Sepsis 3.0 definitions.

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“…CD14 + monocytes inhibited HCV‐induced TRAIL expression on CD56 bright natural killer cells and negatively regulated NK cells activation, predominantly via secretion of interleukin (IL)‐18 and IL‐36 inhibitors . HCV infection increased IL‐1β, IL‐6, and monocyte chemoattractant protein‐1 expression by monocytes/macrophages, which is important for regulation of T cell differentiation and promotion of monocytes migration . However, the modulatory factors to CD14 + monocytes in HCV infection are still not fully elucidated.…”

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confidence: 99%

Notch signaling suppresses CD14⁺ monocytes cells activity in patients with chronic hepatitis C

Zhang

Wang

Zhang

et al. 2019

APMIS

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Z. Notch signaling suppresses CD14 + monocytes cells activity in patients with chronic hepatitis C, APMIS 2019; 127: 642-652.Hepatitis C virus (HCV) infection always leads to chronic hepatitis via dysregulation of host immunity. Notch signaling also modulates the response of monocytes/macrophages. Thus, we aimed to investigate the regulatory role of Notch signaling to CD14 + monocytes. Forty patients with chronic hepatitis C and twenty normal controls (NC) were enrolled. CD14 + monocytes and CD4 + T cells were purified from peripheral bloods. Notch receptors' mRNA expression in CD14 + monocytes was semi-quantified by real-time PCR. Cytokine production by CD14 + monocytes in response to csecretase inhibitor (GSI) was investigated by ELISA. GSI-induced CD14 + monocytes activity to HCV clearance in Huh7.5 cells and to CD4 + T cell differentiation was also assessed in direct and indirect contact co-culture system. Notch1 mRNA relative level was approximately 10-fold elevated in CD14 + monocytes from chronic hepatitis C patients when compared with NC. GSI stimulation resulted in enhanced cytokines production by CD14 + monocytes from chronic hepatitis C patients. GSI-stimulated CD14 + monocytes from chronic hepatitis C patients induced suppression of HCV RNA replication in both direct and indirect contact co-culture system of CD14 + monocytes and HCVcc-infected Huh7.5 cells, and this process was accompanied by elevation of interferon-c production but not increased target cell death. Moreover, GSI stimulation also enhanced CD14 + monocytes-induced Th1 and Th17 cells activation, and this process required direct cell-to-cell contact. Effective antiviral therapy down-regulated Notch1 mRNA expression and promoted cytokine production by CD14 + monocytes from chronic hepatitis C. Current data revealed an important immunoregulatory property of Notch signaling to CD14 + monocytes in chronic HCV infection.

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Monocyte chemoattractant protein 1 released from macrophages induced by hepatitis C virus promotes monocytes migration

Cited by 13 publications

References 33 publications

Influence of hepatitis C virus eradication with direct‐acting antivirals on the gut microbiota in patients with cirrhosis

Influence of hepatitis C virus eradication with direct‐acting antivirals on the gut microbiota in patients with cirrhosis

Plasma PTX3, MCP1 and Ang2 are early biomarkers to evaluate the severity of sepsis and septic shock

Notch signaling suppresses CD14⁺ monocytes cells activity in patients with chronic hepatitis C

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Monocyte chemoattractant protein 1 released from macrophages induced by hepatitis C virus promotes monocytes migration

Cited by 13 publications

References 33 publications

Influence of hepatitis C virus eradication with direct‐acting antivirals on the gut microbiota in patients with cirrhosis

Influence of hepatitis C virus eradication with direct‐acting antivirals on the gut microbiota in patients with cirrhosis

Plasma PTX3, MCP1 and Ang2 are early biomarkers to evaluate the severity of sepsis and septic shock

Notch signaling suppresses CD14+ monocytes cells activity in patients with chronic hepatitis C

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Notch signaling suppresses CD14⁺ monocytes cells activity in patients with chronic hepatitis C