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.
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.
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