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

Song, Xiaotian; Gao, Xiaohan; Wang, Yadong; Raja, Rameez; Zhang, Yaoyu; Yang, Shulin; Li, Miao; Yao, Zhigang; Wei, Lin

doi:10.3389/fimmu.2021.654998

Cited by 16 publications

(11 citation statements)

References 65 publications

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“…In addition, chemokines, C–C motif chemokine ligand (CCL)-2 [ 7 ] and C-X-C motif chemokine ligand (CXCL)-10 [ 8 ], have been reported to be associated with Th1 immune responses. A recent report also found that the induction of CCL2 and CXCL10 secretions in macrophages exaggerated the host-derived immune responses [ 9 ]. Moreover, the heterogeneity of macrophage polarization plays a critical role in several diseases, such as atherosclerosis [ 10 ], pulmonary infection [ 11 ], and obesity-associated metabolic diseases [ 12 ].…”

Section: Introductionmentioning

confidence: 99%

Regulatory Effects of Quercetin on M1/M2 Macrophage Polarization and Oxidative/Antioxidative Balance

et al. 2021

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Macrophage polarization plays essential and diverse roles in most diseases, such as atherosclerosis, adipose tissue inflammation, and insulin resistance. Homeostasis dysfunction in M1/M2 macrophage polarization causes pathological conditions and inflammation. Neuroinflammation is characterized by microglial activation and the concomitant production of pro-inflammatory cytokines, leading to numerous neurodegenerative diseases and psychiatric disorders. Decreased neuroinflammation can be obtained by using natural compounds, including flavonoids, which are known to ameliorate inflammatory responses. Among flavonoids, quercetin possesses multiple pharmacological applications and regulates several biological activities. In the present study, we found that quercetin effectively inhibited the expression of lipocalin-2 in both macrophages and microglial cells stimulated by lipopolysaccharides (LPS). The production of nitric oxide (NO) and expression levels of the pro-inflammatory cytokines, inducible nitric oxide synthase (iNOS) and cyclooxygenase (COX)-2, were also attenuated by quercetin treatment. Our results also showed that quercetin significantly reduced the expression levels of the M1 markers, such as interleukin (IL)-6, tumor necrosis factor (TNF)-α, and IL-1β, in the macrophages and microglia. The M1 polarization-associated chemokines, C–C motif chemokine ligand (CCL)-2 and C-X-C motif chemokine ligand (CXCL)-10, were also effectively reduced by the quercetin treatment. In addition, quercetin markedly reduced the production of various reactive oxygen species (ROS) in the microglia. The microglial phagocytic ability induced by the LPS was also effectively reduced by the quercetin treatment. Importantly, the quercetin increased the expression levels of the M2 marker, IL-10, and the endogenous antioxidants, heme oxygenase (HO)-1, glutamate-cysteine ligase catalytic subunit (GCLC), glutamate-cysteine ligase modifier subunit (GCLM), and NAD(P)H quinone oxidoreductase-1 (NQO1). The enhancement of the M2 markers and endogenous antioxidants by quercetin was activated by the AMP-activated protein kinase (AMPK) and Akt signaling pathways. Together, our study reported that the quercetin inhibited the effects of M1 polarization, including neuroinflammatory responses, ROS production, and phagocytosis. Moreover, the quercetin enhanced the M2 macrophage polarization and endogenous antioxidant expression in both macrophages and microglia. Our findings provide valuable information that quercetin may act as a potential drug for the treatment of diseases related to inflammatory disorders in the central nervous system.

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Section: Introductionmentioning

confidence: 99%

Regulatory Effects of Quercetin on M1/M2 Macrophage Polarization and Oxidative/Antioxidative Balance

et al. 2021

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“…Another worthy topic in this study is that several CXCL family members may have the potential to interact with viral proteins. It was reported that hepatitis C virus (HCV) core protein could induce CXCL10 expression through NF-κB signaling pathway in macrophages [ 46 ]. CXCL10 is a marker of host immune response, which is dependent on interferon (IFN)—γ [ 47 ].…”

Section: Discussionmentioning

confidence: 99%

Genomic Divergence Characterization and Quantitative Proteomics Exploration of Type 4 Porcine Astrovirus

Tao

Cheng

et al. 2022

Viruses

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Porcine astrovirus (PAstV) has been identified as an important diarrheic pathogen with a broad global distribution. The PAstV is a potential pathogen to human beings and plays a role in public health. Until now, the divergence characteristics and pathogenesis of the PAstV are still not well known. In this study, the PAstV-4 strain PAstV/CH/2022/CM1 was isolated from the diarrheal feces of a piglet in Shanghai, which was identified to be a recombination of PAstV4/JPN (LC201612) and PAstV4/CHN (JX060808). A time tree based on the ORF2 protein of the astrovirus demonstrated that type 2–5 PAstV (PAstV-2 to 5) diverged from type 1 PAstV (PAstV-1) at a point from 1992 to 2000. To better understand the molecular basis of the virus, we sought to explore the host cell response to the PAstV/CH/2022/CM1 infection using proteomics. The results demonstrate that viral infection elicits global protein changes, and that the mitochondria seems to be a primary and an important target in viral infection. Importantly, there was crosstalk between autophagy and apoptosis, in which ATG7 might be the key mediator. In addition, the NOD-like receptor X1 (NLRX1) in the mitochondria was activated and participated in several important antiviral signaling pathways after the PAstV/CH/2022/CM1 infection, which was closely related to mitophagy. The NLRX1 may be a crucial protein for antagonizing a viral infection through autophagy, but this has yet to be validated. In conclusion, the data in this study provides more information for understanding the virus genomic characterization and the potential antiviral targets in a PAstV infection.

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“…It has been shown that STAT1 may reduce liver fibrosis by inhibiting HSC proliferation and stimulating NK cells to destroy activated HSC ( 26 ). CXCL10 can have an expressional induction after viral stimulation of the liver ( 27 ). Several studies have suggested that CXCL10 is associated with viral liver fibrosis ( 28 , 29 ).…”

Section: Discussionmentioning

confidence: 99%

Exploration of immune infiltration and feature genes in viral hepatitis-associated liver fibrosis using transcriptome data

Pan¹,

Tian²,

Hu³

et al. 2022

Ann Transl Med

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Background: Immune cells play an essential role in virus-induced liver fibrosis. However, the underlying mechanisms remain unclear. In this study, we systematically explored immune cell infiltration and feature genes to provide new insights into viral hepatitis-associated liver fibrosis. Methods:The expression datasets GSE14323, GSE33650, GSE6764 (for testing), and GSE84044 (for validation) were downloaded from the Gene Expression Omnibus (GEO) database. Immune cell infiltration was assessed using the CIBERSORT algorithm, and characteristic subgroups were obtained using least absolute shrinkage and selection operator (LASSO) regression and Wilcox Text. The association between feature genes and immune-infiltrating cells was explored using Spearman's correlation analysis. R software and IBM SPSS Statistics were utilized for data analysis and visualization.Results: We identified 10 differential immune cells between viral hepatitis-associated liver fibrosis and non-fibrosis, including naive B cells, plasma cells, resting CD4+ memory T cells, T follicular helper (Tfh) cells, regulatory T (Treg) cells, M0-M2 macrophages, and resting and activated mast cells. Six feature genes were identified: STAT1, CXCL10, PTPRC, IFIT3, OAS2, and MX1. They also differed significantly in the subgroups of non-fibrosis, mild to moderate fibrosis and severe fibrosis. Both the feature genes and immune cells were verified in the validation group. All the genes were positively associated with macrophages M1 and negatively associated with macrophages M2. Conclusions:The six feature genes may be involved in viral hepatitis-associated liver fibrosis by promoting the polarization of macrophages from M0 to M1 and inhibiting their conversion to M2. Thus, these genes may serve as potential therapeutic targets.

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

Cited by 16 publications

References 65 publications

Regulatory Effects of Quercetin on M1/M2 Macrophage Polarization and Oxidative/Antioxidative Balance

Regulatory Effects of Quercetin on M1/M2 Macrophage Polarization and Oxidative/Antioxidative Balance

Genomic Divergence Characterization and Quantitative Proteomics Exploration of Type 4 Porcine Astrovirus

Exploration of immune infiltration and feature genes in viral hepatitis-associated liver fibrosis using transcriptome data

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