scholarly journals Plasma Inflammatory Biomarkers Associated with Advanced Liver Fibrosis in HIV–HCV-Coinfected Individuals

2020 ◽  
Vol 17 (24) ◽  
pp. 9474
Author(s):  
Xiaochen Chen ◽  
Xing Liu ◽  
Song Duan ◽  
Renhai Tang ◽  
Sujuan Zhou ◽  
...  
Keyword(s):  
Liver Fibrosis ◽  
Plasma Concentrations ◽  
Clinical Intervention ◽  
Interferon Γ ◽  
Microbial Translocation ◽  
Cross Sectional ◽  
Monocyte Chemoattractant Protein 1 ◽  
Gm Csf ◽  
Advanced Liver Fibrosis ◽  
Ifn Γ

Background: HIV and HCV coinfection leads to accelerated liver fibrosis, in which microbial translocation and systemic inflammation might play important roles. Objective: This study aimed to provide an extensive profile of the plasma microbial translocation and inflammation biomarkers associated with advanced liver fibrosis among HIV–HCV-coinfected patients. Methods: This cross-sectional study recruited 343 HIV–HCV-coinfected patients on combination antiretroviral therapy (cART) from a rural prefecture of Yunnan province in Southwest China. The plasma concentrations of sCD14 and 27 cytokines and chemokines were assayed and compared against advanced or mild levels of liver fibrosis. Results: Of the 343 HIV–HCV-coinfected patients, 188 (54.8%) had severe or advanced liver fibrosis (FIB-4 > 3.25). The patients with advanced liver fibrosis (FIB-4 > 3.25 vs. FIB-4 ≤ 3.25) had higher plasma levels of interleukin (IL)-1β, IL-6, IL-7, IL-9, IL-12, IL-15, IL-17, granulocyte macrophage colony stimulating factor (GM-CSF), Interferon-γ (IFN-γ), tumor necrosis factor (TNF-α), IL-4, IL-10, IL-13, fibroblast growth factor 2 (FGF-basic), and Monocyte chemoattractant protein-1 (MCP-1). Multivariable logistic regression models showed that advanced liver fibrosis was associated with an increased plasma level of IL-1β, IL-6, IL-7, IL-12, IL-17, GM-CSF, IFN-γ, IL-4, IL-10, MCP-1, Eotaxin, and FGF-basic, with FGF-basic continuing to be positively and significantly associated with advanced liver fibrosis, after Bonferroni correction for multiple comparisons (adjusted odds ratio (aOR) = 1.92; 95%CI: 1.32–2.81; p = 0.001). Plasma sCD14 was also significantly associated with advanced liver fibrosis (aOR = 1.13; 95%CI: 1.01–1.30; p = 0.049). Conclusions: HIV–HCV-coinfected patients are living with a high prevalence of advanced liver fibrosis which coexists with a mixture of elevated plasma inflammation and microbial translocation biomarkers. The significant associations of advanced liver fibrosis with FGF-basic and sCD14 may reveal pathogenic mechanisms and potential clinical intervention targets for liver fibrosis in HCV–HIV coinfection.

scholarly journals Profiling Circulating Inflammation and Microbial Translocation Biomarkers Associated with Advanced Liver Fibrosis in HIV/HCV Coinfected Persons

2020 ◽  
Author(s):  
Xiaochen Chen ◽  
Xing Liu ◽  
Song Duan ◽  
Renhai Tang ◽  
Sujuan Zhou ◽  
...  
Keyword(s):  
Liver Fibrosis ◽  
Plasma Concentrations ◽  
Clinical Intervention ◽  
Cross Sectional Study ◽  
Microbial Translocation ◽  
Cross Sectional ◽  
Logistic Regression Models ◽  
Gm Csf ◽  
Advanced Liver Fibrosis ◽  
Ifn Γ

Abstract Background: HIV/HCV coinfection leads to accelerated liver fibrosis, in which microbial translocation and systemic inflammation might play important roles. This study aimed to provide an extensive profile of plasma microbial translocation and inflammation biomarkers associated with advanced liver fibrosis among HIV/HCV coinfected patients.Methods:This cross-sectional study recruited 343 HIV/HCV coinfected patients on combination antiretroviral therapy (cART) from a rural prefecture of Yunnan province in Southwest China. Plasma concentrations of sCD14 and 27 cytokines/chemokines were assayed, and were compared against advanced or mild levels of liver fibrosis.Results: Of the 343 HIV/HCV coinfected patients, 188 (54.8%) had severe or advanced liver fibrosis (FIB-4 >3.25). Patients with advanced liver fibrosis (FIB-4 >3.25 vs. FIB-4 ≤3.25) had higher plasma levels of IL-1β, IL-6, IL-7, IL-9, IL-12, IL-15, IL-17, GM-CSF, IFN-γ, TNF-α, IL-4, IL-10, IL-13, FGF-basic and MCP-1. Multivariable logistic regression models showed that advanced liver fibrosis was associated with increased plasma level of IL-1β, IL-6, IL-7, IL-12, IL-17, GM- CSF, IFN-γ, IL-4, IL -10, MCP-1, Eotaxin and FGF-basic, with FGF-basic remained to be positively and significantly associated with advanced liver fibrosis after Bonferroni correction for multiple comparisons (aOR=1.82; 95%CI: 1.26-2.66; p=0.002). Plasma sCD14 was also significantly associated with advanced liver fibrosis (aOR=1.14; 95%CI: 1.01-1.30; p=0.048).Conclusions: HIV/HCV coinfected patients are living with high prevalence of advanced liver fibrosis which coexists with a mixture of elevated plasma inflammation and microbial translocation biomarkers. The significant associations of advanced liver fibrosis with FGF-basic and sCD14 may reveal pathogenic mechanisms and potential clinical intervention targets of liver fibrosis in HCV/HIV coinfection.

scholarly journals Severe Liver Fibrosis and Association with Plasma Inflammatory Biomarkers among HIV/HCV Co-infected Patients in China :a Cross-Sectional Study

2019 ◽  
Author(s):  
Xiaochen Chen ◽  
Xing Liu ◽  
Song Duan ◽  
Renhai Tang ◽  
Sujuan Zhou ◽  
...  
Keyword(s):  
Logistic Regression ◽  
Liver Fibrosis ◽  
Plasma Level ◽  
Cross Sectional Study ◽  
Inflammatory Biomarkers ◽  
Sectional Study ◽  
Severe Liver ◽  
Cross Sectional ◽  
Gm Csf ◽  
Ifn Γ

Abstract Background: Immune dysregulation among HIV/HCV co-infected patients with impaired liver function is common. Thus, this study aimed to evaluate the association of liver fibrosis with microbial translocation and related inflammation among HIV/HCV co-infected patients. Methods: This cross-sectional study involved 343 HIV/HCV co-infected patients who received cART. All patients had current blood biochemical testing data. We measured sCD14 and 27 serum cytokines concentrations using the Hycult Biotech sCD14 ELISA kit and Bio-plex Human Cytokine 27-plex Assay, respectively. We compared the concentrations of each marker between severe liver fibrosis and mild liver fibrosis. Odds ratios (ORs) and 95% confidence intervals (95%CIs) for the association of each marker with severe liver fibrosis were estimated using logistic regression. Results: Of the 343 HIV/HCV coinfect-ed patients enrolled, 188 (54.8%) had severe liver fibrosis (FIB-4 >3.25). Patients with higher FIB-4 score (>3.25vs. ≤3.25) had higher plasma level of IL-1β, IL-6, IL-7, IL-9, IL-12, IL-15, IL-17, GM-CSF, IFN-γ, TNF-α, IL-4, IL-10, IL-13, BasicFGF and MCP-1. Multivariate logistic regression analysis showed that increased plasma level of IL-1β, IL-6, IL-7, IL-12, IL-17, GM- CSF, IFN-γ, IL-4, IL -10, MCP-1, Eotaxin, BasicFGF and sCD14 were linked to severe liver fibrosis in our study. Conclusions: Severe liver fibrosis are associated with increased microbial translocation plasma inflammatory biomarkers among HIV/HCV co-infected patients.

Clinical significance of cytokine markers in children with different courses of community-acquired pneumonia

2020 ◽  
Vol 15 (5) ◽  
pp. 18-23
Author(s):  
G.P. Evseeva ◽  
◽  
G.N. Kholodok ◽  
S.V. Pichugina ◽  
S.V. Suprun ◽  
...  
Keyword(s):  
Cytokine Production ◽  
Interleukin 1 ◽  
Interferon Γ ◽  
Peripheral Blood Lymphocytes ◽  
Community Acquired Pneumonia ◽  
Enzyme Linked Immunosorbent Assay ◽  
Interleukin 17 ◽  
Monocyte Chemoattractant Protein 1 ◽  
Tnf Α ◽  
Ifn Γ

Principles of the diagnosis and treatment of community-acquired pneumonia (CAP) in children were developed and clearly formulated long ago. Nevertheless, clinicians often encounter the problem of pulmonary and pleural complications of CAP, which is challenging in terms of the choice of initial therapy, since the first symptoms of uncomplicated and complicated pneumonia are often similar. Therefore, the search for early markers of complicated CAP in children is highly important. Objective. To assess prognostic values of spontaneous and mitogen-induced cytokine production in children with CAP. Patients and methods. We have performed comprehensive examination of 108 children with CAP. Eighty-four of them had uncomplicated CAP, whereas 24 children had CAP complicated by pleurisy. We measured spontaneous and induced production of the following cytokines upon patient admission to hospital: interleukin-1 (IL-1), interleukin-17 (IL-17), interferon-γ (IFN-γ), tumor necrosis factor-α (TNF-α), vascular endothelial growth factor (VEGF), and monocyte chemoattractant protein-1 (MCP-1). To measure induced cytokine production, we stimulated peripheral blood lymphocytes by S. рneumonае (serotype 7, 11; strains 7C and 11AD). The level of cytokines was evaluated using the enzyme-linked immunosorbent assay (Vektor-BEST, Novosibirsk, Russia). Results. We found that in children with uncomplicated CAP, induction of immunocompetent blood cells (IBCs) led to increased secretion of first-generation cytokines, including IL-1, TNF-α, and IFN-γ, whereas IBCs of patients with complicated CAP primarily produced second-generation cytokines, including VEGF, МРС-1, and IL-17. Conclusion. The observed differences in spontaneous and mitogen-induced cytokine production between children with and without CAP complications suggest that these parameters can be considered as promising prognostic markers for complicated CAP in children. The proposed method can be used in pediatric practice to predict the development of complications in children with CAP. Key words: children, community-acquired pneumonia, cytokines

Cytokines and chemokines triggered by Chikungunya virus infection in human patients during the very early acute phase

2019 ◽  
Vol 113 (11) ◽  
pp. 730-733 ◽  
Author(s):  
Ithallo S B Tanabe ◽  
Elane C Santos ◽  
Eloiza L L Tanabe ◽  
Stephannie J M Souza ◽  
Fabio E F Santos ◽  
...  
Keyword(s):  
Immune Response ◽  
Acute Phase ◽  
Chikungunya Virus ◽  
Interleukin 10 ◽  
Interferon Γ ◽  
Interferon Α ◽  
Monocyte Chemoattractant Protein 1 ◽  
Illness Onset ◽  
Ifn Γ ◽  
C5a Anaphylatoxin

Abstract Background The immune response against the Chikungunya virus (CHIKV) during the very early acute phase is not fully elucidated. Therefore we explored the cytokine and chemokine profile triggered by CHIKV in infected patients. Methods Cytokines, chemokines and C5a anaphylatoxin were analysed in serum from CHIKV-infected patients during the viraemic phase (mean 2.97±1.27 d after illness onset) compared with a healthy group. Results CHIKV-infected patients had a significant increase of interferon-α (IFN-α), interleukin-6 (IL-6), interleukin-8 (CXCL8/IL-8), interleukin-10 (IL-10), interferon-γ (IFN-γ), monokine induced by interferon-γ (CXCL9/MIG), monocyte chemoattractant protein-1 (CCL2/MCP-1), interferon-γ-induced protein-10 (CXCL10/IP-10) and complement C5a anaphylatoxin. Conclusions The very early acute immune response triggered against CHIKV leads to an increase in pro-inflammatory immune mediators such as IFN-γ and its induced chemokines, and a high level of C5a anaphylatoxin as a result of complement activation.

Interferon-γ switches monocyte differentiation from dendritic cells to macrophages

Blood ◽  
2003 ◽  
Vol 101 (1) ◽  
pp. 143-150 ◽  
Author(s):  
Yves Delneste ◽  
Peggy Charbonnier ◽  
Nathalie Herbault ◽  
Giovanni Magistrelli ◽  
Gersende Caron ◽  
...  
Keyword(s):  
Dendritic Cells ◽  
Interferon Γ ◽  
Transcriptional Level ◽  
Colony Stimulating Factor ◽  
Monocyte Differentiation ◽  
Gm Csf ◽  
Macrophage Colony Stimulating Factor ◽  
Ifn Γ ◽  
Macrophage Colony ◽  
Stimulating Factor

Abstract Human monocytes differentiate into dendritic cells (DCs) or macrophages according to the nature of environmental signals. Monocytes stimulated with granulocyte-macrophage colony-stimulating factor (GM-CSF) plus interleukin 4 (IL-4) yield DCs. We tested here whether interferon-γ (IFN-γ), a potent activator of macrophages, may modulate monocyte differentiation. Addition of IFN-γ to IL-4 plus GM-CSF–stimulated monocytes switches their differentiation from DCs to CD14−CD64+ macrophages. IFN-γ increases macrophage colony-stimulating factor (M-CSF) and IL-6 production by IL-4 plus GM-CSF–stimulated monocytes by acting at the transcriptional level and acts together with IL-4 to up-regulate M-CSF but not IL-6 production. IFN-γ also increases M-CSF receptor internalization. Results from neutralizing experiments show that both M-CSF and IL-6 are involved in the ability of IFN-γ to skew monocyte differentiation from DCs to macrophages. Finally, this effect of IFN-γ is limited to early stages of differentiation. When added to immature DCs, IFN-γ up-regulates IL-6 but not M-CSF production and does not convert them to macrophages, even in the presence of exogenous M-CSF. In conclusion, IFN-γ shifts monocyte differentiation to macrophages rather than DCs through autocrine M-CSF and IL-6 production. These data show that IFN-γ controls the differentiation of antigen-presenting cells and thereby reveals a new mechanism by which IFN-γ orchestrates the outcome of specific immune responses.

scholarly journals Cytokine regulation of stem cells

2016 ◽  
Author(s):  
Gyanesh Singh ◽  
Hasan Korkaya
Keyword(s):  
Stem Cells ◽  
Dendritic Cells ◽  
Stem Cell ◽  
Immune Cells ◽  
Interferon Γ ◽  
Gm Csf ◽  
Cell Functions ◽  
Tnf Α ◽  
Different Types ◽  
Ifn Γ

Different types of stem cells are targeted by a number of cytokines that alter proliferation, differentiation, or other properties of stem cells. Stem cells are known to express various cytokine genes. As IL-12, IL-14, G-CSF, and GM-CSF expression is lost after the differentiation of MSCs, these factors might have major contribution to pluripotency. Several other cytokines that are produced by immune cells, frequently target stem cells. Modulation of stem cell functions by cytokines can be a cause of various diseases including cancer. Stem cells can show immunosuppressive properties by a number of mechanisms. MSC-induced immunosuppression is often mediated by IFN-γ, TNF-α, IL-1α, or IL-1β. In co-culture experiments, MSCs were able to control T cells IL-2 response, or, dendritic cells TNF-α and IL-10 secretion. MSCs are also known to cause decreased interferon γ (IFN-γ) and increased IL-4 production by immune cells. However, the outcome in most of the cases depends on the presence of various factors that might synergize or antagonize with each other.

scholarly journals Cotinine and interferon-gamma levels in pre-school children exposed to household tobacco smoke

2016 ◽  
Vol 53 (5) ◽  
pp. 287
Author(s):  
Lina Kalalo ◽  
Diana Takumansang-Sondakh ◽  
Audrey Wahani
Keyword(s):  
Tobacco Smoke ◽  
Interferon Γ ◽  
Cross Sectional Study ◽  
Smoke Exposure ◽  
Tobacco Smoke Exposure ◽  
Healthy Children ◽  
Exposure Group ◽  
Serum Cotinine ◽  
Cross Sectional ◽  
Ifn Γ

Background Environmental tobacco smoke has been consistently linked to negative health outcomes, especially in children, including an increased susceptibility to infections. Cigarette smoking has a depressive effect on interferon-γ (IFN-γ). Serum cotinine is a marker of exposure to smoke.Objective To determine the association between serum cotinine and interferon-γ (IFN-γ) levels in children with household tobacco smoke exposure.Methods We conducted a cross-sectional study at the Tumumpa and Singkil Districts of Manado, Indonesia, from February to May 2012. Subjects were collected by consecutively sampling of healthy children aged 1-3 years who came to the integrated health posts. Seventy-four children were recruited and consisted of two groups of 37 subjects each, the tobacco smoke exposure group and the non-tobacco smoke exposure group. Blood specimens were collected from all subjects for laboratory blood tests of cotinine and IFN-γ levels. Results were analyzed by T-test and Pearson’s correlation analysis with a P<0.05 is considered as statistically significant.Results There was no significant correlation between serum cotinine and interferon-γ levels in the tobacco smoke exposure group. However, the interferon-γ level in the tobacco smoke exposure group was significantly lower than that of the non-tobacco smoke exposure group (P<0.0001).Conclusion Cotinine is not related to the interferon-γ level in children exposed to tobacco smoke, however, the interferon-γ level in children with tobacco smoke exposure is lower than in the non-tobacco smoke exposure group.

scholarly journals CXC chemokine receptor 3 expression on CD34+hematopoietic progenitors from human cord blood induced by granulocyte-macrophage colony-stimulating factor: chemotaxis and adhesion induced by its ligands, interferon γ–inducible protein 10 and monokine induced by interferon γ

Blood ◽  
2000 ◽  
Vol 96 (4) ◽  
pp. 1230-1238 ◽  
Author(s):  
Tan Jinquan ◽  
Sha Quan ◽  
Henrik H. Jacobi ◽  
Chen Jing ◽  
Anders Millner ◽  
...  
Keyword(s):  
Interferon Γ ◽  
Colony Stimulating Factor ◽  
Hematopoietic Progenitors ◽  
Human Cord Blood ◽  
Gm Csf ◽  
Macrophage Colony Stimulating Factor ◽  
Ifn Γ ◽  
Inducible Protein ◽  
Macrophage Colony ◽  
Stimulating Factor

Abstract CXC chemokine receptor 3 (CXCR3), which is known to be expressed predominately on memory and activated T lymphocytes, is a receptor for both interferon γ (IFN-γ)–inducible protein 10 (γIP-10) and monokine induced by IFN-γ (Mig). We report the novel finding that CXCR3 is also expressed on CD34+ hematopoietic progenitors from human cord blood stimulated with granulocyte-macrophage colony-stimulating factor (GM-CSF) but not on freshly isolated CD34+ progenitors. Freshly isolated CD34+progenitors expressed low levels of CXCR3 messenger RNA, but this expression was highly up-regulated by GM-CSF, as indicated by a real-time quantitative reverse transcriptase–polymerase chain reaction technique. γIP-10 and Mig induced chemotaxis of GM-CSF–stimulated CD34+ progenitors by means of CXCR3, since an anti-CXCR3 monoclonal antibody (mAb) was found to block γIP-10–induced and Mig-induced CD34+ progenitor chemotaxis. These chemotactic attracted CD34+ progenitors are colony-forming units—granulocyte-macrophage. γIP-10 and Mig also induced GM-CSF–stimulated CD34+ progenitor adhesion and aggregation by means of CXCR3, a finding confirmed by the observation that anti-CXCR3 mAb blocked these functions of γIP-10 and Mig but not of chemokine stromal cell–derived factor 1α. γIP-10–induced and Mig-induced up-regulation of integrins (CD49a and CD49b) was found to play a crucial role in adhesion of GM-CSF–stimulated CD34+progenitors. Moreover, γIP-10 and Mig stimulated CXCR3 redistribution and cellular polarization in GM-CSF–stimulated CD34+progenitors. These results indicate that CXCR3–γIP-10 and CXCR3–Mig receptor-ligand pairs, as well as the effects of GM-CSF on them, may be especially important in the cytokine/chemokine environment for the physiologic and pathophysiologic events of differentiation of CD34+ hematopoietic progenitors into lymphoid and myeloid stem cells, subsequently immune and inflammatory cells. These processes include transmigration, relocation, differentiation, and maturation of CD34+ hematopoietic progenitors.

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