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Dynamic changes in the frequency of classical CD14HighCD16- and inflammatory CD14++CD16+ monocyte subsets in patients
Pedro V da Silva-Neto1, Grenda L Pereira2, Priscila S Souza2
1Universidade Federal do Amazonas (UFAM), Manaus 69067-005, AM, Brazil; Programa de Pós-Graduação em Imunologia Básica e Aplicada - PPGIBA, Instituto de Ciências Biológicas, Universidade Federal do Amazonas- UFAM, Manaus 69080-900, AM, Brazil; Departamento de Análises Clínicas, Toxicológicas e Bromatológicas, Faculdade de Ciências Farmacêuticas de Ribeirão Preto-FCFRP, Universidade de São Paulo-USP, Ribeirão Preto 14040-903, SP, Brazil; Programa de Pós-Graduação em Ciências Aplicadas à Hematologia, Universidade do Estado do Amazonas (UEA), Manaus 69065-001, AM, Brazil.
Insights
Chronic Hepatitis C (HCV) infection alters monocyte subsets and inflammatory markers, particularly in severe liver fibrosis. These changes impact cellular activation and are linked to increased pro-inflammatory mediators.
Area of Science:
- Immunology
- Hepatology
- Virology
Background:
- Hepatitis C (HCV) affects millions globally, causing chronic inflammation.
- Inflammatory mediators influence monocyte phenotypes during chronic infection.
- Understanding monocyte subset changes in HCV with fibrosis is crucial.
Purpose of the Study:
- Investigate peripheral monocyte subset phenotypes in Brazilian Amazon patients with chronic HCV.
- Analyze circulating mediators in relation to liver fibrosis severity.
- Determine the impact of HCV on monocyte activation markers.
Main Methods:
- Observational study of 30 HCV patients and 15 controls.
- Assessed liver function, fibrosis scores (AST/platelet ratio index, FIB-4).
- Analyzed monocyte subsets (CD14/CD16 expression) and immunological biomarkers via flow cytometry.
Main Results:
- HCV patients with high fibrosis (FIB-4 ≥ F2) had lower platelets and elevated viral load, ALT, AST, and alkaline phosphatase.
- Decreased frequency of CD14HighCD16-HLA-DR+ cells observed.
- Increased inflammatory CD14++CD16+HLA-DR+ monocytes showed higher expression of integrins (CD11a, CD11b), activation markers (CD49d), and P2X7 receptor.
Conclusions:
- Chronic HCV infection significantly alters peripheral inflammatory monocyte subsets.
- These alterations impact cellular markers and activation, especially in severe liver impairment (FIB-4 ≥ F2).
- Soluble biomarkers are linked to pro-inflammatory monocyte phenotypes, contributing to inflammation and fibrosis in HCV.
Abstract:
Hepatitis C is a global health problem, with approximately 71 million individuals chronically infected worldwide. During chronic inflammatory processes, the elevated expression of inflammatory mediators appears to influence the phenotype of circulating monocytes. Our objective was to investigate changes in the phenotypes of peripheral monocyte subsets and the profile of circulating mediators in patients from the Brazilian Amazon during chronic hepatitis C and associated with different degrees of liver fibrosis.
Material And Methods:
This is an observational study involving 30 individuals treated with DAAs and 15 healthy controls, tested for liver function, fibrosis scores (AST/platelet ratio index, FIB-4), percentage of peripheral blood monocyte subsets assessed with based on CD14/CD16 expression. The analysis of soluble immunological biomarkers was performed using the flow cytometry methodology.
Results:
Chronic HCV patients showed decreased platelet counts and increased viral load, ALT, AST, alkaline phosphatase in individuals with high fibrosis scores (FIB-4 ≥ F2). Data analysis demonstrated a lower frequency of CD14HighCD16-HLA-DR+ cells, while inflammatory CD14++CD16+HLA-DR+ monocytes increased the expression of CD11a and CD11b integrins, CD49d activation markers, and the inflammatory receptor P2X7. Serum cytokine expression showed that liver fibrosis is associated with higher serum levels of IL-6, CXCL8, and CXCL9 compared to mild liver disease.
Conclusions:
In conclusion, our findings demonstrated that Chronic HCV infection alters the frequency of peripheral inflammatory monocyte subsets, impacting cellular markers and activation in severe liver impairment (FIB-4 ≥ F2). Soluble biomarkers modulate pro-inflammatory monocyte phenotypes, linked to inflammation and fibrosis.
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