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Monitoring Changes in Human Umbilical Vein Endothelial Cells upon Viral Infection Using Impedance-Based Real-Time Cell Analysis
Published on: May 5, 2023
796
High dengue virus load differentially modulates human microvascular endothelial barrier function during early
Hui Jen Soe1, Asif M Khan2, Rishya Manikam3
1Department of Medical Microbiology, Faculty of Medicine, University of Malaya, Kuala Lumpur, Malaysia.
The Journal of General Virology
|November 29, 2017
Summary
Severe dengue causes plasma leakage by damaging vascular barriers. This study shows dengue virus differentially affects human microvascular endothelial cells, altering barrier function and cytokine production, highlighting organ-specific responses.
Area of Science:
- Vascular biology
- Immunology
- Virology
Background:
- Plasma leakage is a hallmark of severe dengue, stemming from compromised vascular barrier integrity and dysregulated immune responses.
- Understanding the specific mechanisms of vascular dysfunction in different human microvascular endothelial cells (MECs) is crucial for dengue pathogenesis research.
Purpose of the Study:
- To investigate the functional changes in four human MEC lines (brain, dermal, pulmonary, retinal) upon dengue virus infection.
- To assess the impact of dengue virus on cytokine profiles and inter-endothelial junctional proteins.
- To evaluate the influence of virus stock purity on dengue-specific immune responses.
Main Methods:
- Utilized electric cell-substrate impedance sensing (ECIS) to model vascular leakage in infected MECs.
- Analyzed cytokine profiles and expression of junctional proteins (ZO-1, claudin-1, PECAM-1, VE-cadherin).
- Compared responses using purified and non-purified dengue virus stocks.
Main Results:
- Vascular leakage in dengue-infected MECs is primarily due to altered cell-to-cell interactions, with variations across cell lines and DENV serotypes.
- Differential production of inflammatory cytokines (IL-6, TNF-α), chemokines, and adhesion molecules (VCAM-1) was observed.
- Down-regulation of ZO-1 and differential expression of other junctional proteins occurred in specific infected MECs.
- Non-purified virus stocks may confound dengue-specific immune responses.
Conclusions:
- High dengue virus load differentially modulates human microvascular endothelial barrier function.
- Disruption of inter-endothelial junctional proteins and organ-specific cytokine production are key features of early dengue infection.
- Virus stock purity is a critical factor to consider in dengue research.
