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Peer-reviewedCC BY 4.0Frontiers in Immunology

Endothelial injury and acute-phase inflammatory mediators converge to drive dengue severity

  • Abdul R. Anshad1
  • Muthuvel Atchaya1
  • Shanmugam Saravanan2
  • Amudhan Murugesan3
  • Pachamuthu Balakrishnan4
  • Sivadoss Raju5
  • Yean K. Yong6
  • Marie Larsson7
  • Esaki M. Shankar1
7 affiliations
  1. 1Infection and Inflammation, Department of Biotechnology, Central University of Tamil Nadu, Neelakudi
  2. 2Dental Research Cell, Dr. D. Y. Patil Dental College and Hospital, Dr. D. Y. Patil Vidyapeeth, Pune
  3. 3Deparment of Microbiology, The Government Theni Medical College and Hospital
  4. 4Department of Research, Meenakshi Academy of Higher Education and Research
  5. 5State Public Health Laboratory, Directorate of Public Health and Preventive Medicine
  6. 6Laboratory Center, Xiamen University Malaysia
  7. 7Molecular Medicine and Virology, Department of Biomedical and Clinical Sciences, Linköping University
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Abstract

Introduction: Severe dengue infection is characterized by endothelial injury and systemic inflammatory complications. To better understand the mechanisms underlying disease severity, we investigated a broad panel of circulating inflammatory and endothelial mediators in patients with clinical dengue infection.

Methods: A prospective cross-sectional study was carried out involving 111 dengue patients and 42 healthy controls. Among the dengue cases, 85 were identified as primary, while 26 were classified as secondary dengue infections. Serum levels of endothelial markers (Ang-2, CXCL10, MCP1, and TRAIL), liver dysfunction and acute-phase markers (CRP, galectin 3, and serum amyloid protein), systemic inflammatory mediators (MIF, TNF-α, IL-1β), mast cell-derived proteases (chymase, tryptase), and tissue repair markers HGF, IL-10, IL-1Ra) were quantified using ELISA and Luminex multiplex assays. Correlations among serum analytes, severity indicators, and haematological markers were also explored.

Results: Several biomarkers, Ang-2, CXCL10, TRAIL, CRP, MIF, IL-1Ra, TNF-α, and chymase showed differential expression across severity groups, indicating coordinated endothelial and inflammatory activation. Stratification of patients with primary-secondary dengue also followed a similar pattern except IL-1β, which had significant differential expression across the cohorts. Ang‐2 showed strong positive correlations with markers of hepatic dysfunction, including ALT, AST, and bilirubin, suggesting a link between endothelial injury and liver involvement.

Conclusions: Severe dengue is driven by the coordinated activation of endothelial dysfunction, acute-phase responses, mast cell mediators, and counter-regulatory pathways. These processes collectively contribute to vascular leakage and organ injury, reinforcing the value of biomarkers such as Ang-2, CXCL10, CRP, and chymase for severity assessment.

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Cite

BibTeXRIS
BibTeX
@article{anshad2026endothelial,
  title = {{Endothelial injury and acute-phase inflammatory mediators converge to drive dengue severity}},
  author = {Abdul R. Anshad and Muthuvel Atchaya and Shanmugam Saravanan and Amudhan Murugesan and Pachamuthu Balakrishnan and Sivadoss Raju and Yean K. Yong and Marie Larsson and Esaki M. Shankar},
  journal = {Frontiers in Immunology},
  year = {2026},
  month = oct,
  doi = {10.3389/fimmu.2026.1970274},
  url = {https://www.frontiersin.org/articles/10.3389/fimmu.2026.1970274/full},
  note = {CC BY 4.0},
}
RIS
TY  - JOUR
TI  - Endothelial injury and acute-phase inflammatory mediators converge to drive dengue severity
AU  - Abdul R. Anshad
AU  - Muthuvel Atchaya
AU  - Shanmugam Saravanan
AU  - Amudhan Murugesan
AU  - Pachamuthu Balakrishnan
AU  - Sivadoss Raju
AU  - Yean K. Yong
AU  - Marie Larsson
AU  - Esaki M. Shankar
PY  - 2026
DA  - 2026/10/08
JO  - Frontiers in Immunology
DO  - 10.3389/fimmu.2026.1970274
UR  - https://www.frontiersin.org/articles/10.3389/fimmu.2026.1970274/full
AB  - Introduction: Severe dengue infection is characterized by endothelial injury and systemic inflammatory complications. To better understand the mechanisms underlying disease severity, we investigated a broad panel of circulating inflammatory and endothelial mediators in patients with clinical dengue infection.  Methods: A prospective cross-sectional study was carried out involving 111 dengue patients and 42 healthy controls. Among the dengue cases, 85 were identified as primary, while 26 were classified as secondary dengue infections. Serum levels of endothelial markers (Ang-2, CXCL10, MCP1, and TRAIL), liver dysfunction and acute-phase markers (CRP, galectin 3, and serum amyloid protein), systemic inflammatory mediators (MIF, TNF-α, IL-1β), mast cell-derived proteases (chymase, tryptase), and tissue repair markers HGF, IL-10, IL-1Ra) were quantified using ELISA and Luminex multiplex assays. Correlations among serum analytes, severity indicators, and haematological markers were also explored.  Results: Several biomarkers, Ang-2, CXCL10, TRAIL, CRP, MIF, IL-1Ra, TNF-α, and chymase showed differential expression across severity groups, indicating coordinated endothelial and inflammatory activation. Stratification of patients with primary-secondary dengue also followed a similar pattern except IL-1β, which had significant differential expression across the cohorts. Ang‐2 showed strong positive correlations with markers of hepatic dysfunction, including ALT, AST, and bilirubin, suggesting a link between endothelial injury and liver involvement.  Conclusions: Severe dengue is driven by the coordinated activation of endothelial dysfunction, acute-phase responses, mast cell mediators, and counter-regulatory pathways. These processes collectively contribute to vascular leakage and organ injury, reinforcing the value of biomarkers such as Ang-2, CXCL10, CRP, and chymase for severity assessment.
SN  - 1664-3224
ER  -