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The Disruption of the Endothelial Barrier Contributes to Acute Lung Injury Induced by Coxsackievirus A2 Infection in Mice.

Publication ,  Journal Article
Ji, W; Hu, Q; Zhang, M; Zhang, C; Chen, C; Yan, Y; Zhang, X; Chen, S; Tao, L; Zhang, W; Jin, Y; Duan, G
Published in: Int J Mol Sci
September 13, 2021

Sporadic occurrences and outbreaks of hand, foot, and mouth disease (HFMD) caused by Coxsackievirus A2 (CVA2) have frequently reported worldwide recently, which pose a great challenge to public health. Epidemiological studies have suggested that the main cause of death in critical patients is pulmonary edema. However, the pathogenesis of this underlying comorbidity remains unclear. In this study, we utilized the 5-day-old BALB/c mouse model of lethal CVA2 infection to evaluate lung damage. We found that the permeability of lung microvascular was significantly increased after CVA2 infection. We also observed the direct infection and apoptosis of lung endothelial cells as well as the destruction of tight junctions between endothelial cells. CVA2 infection led to the degradation of tight junction proteins (e.g., ZO-1, claudin-5, and occludin). The gene transcription levels of von Willebrand factor (vWF), endothelin (ET), thrombomodulin (THBD), granular membrane protein 140 (GMP140), and intercellular cell adhesion molecule-1 (ICAM-1) related to endothelial dysfunction were all significantly increased. Additionally, CVA2 infection induced the increased expression of inflammatory cytokines (IL-6, IL-1β, and MCP-1) and the activation of p38 mitogen-activated protein kinase (MAPK). In conclusion, the disruption of the endothelial barrier contributes to acute lung injury induced by CVA2 infection; targeting p38-MAPK signaling may provide a therapeutic approach for pulmonary edema in critical infections of HFMD.

Duke Scholars

Published In

Int J Mol Sci

DOI

EISSN

1422-0067

Publication Date

September 13, 2021

Volume

22

Issue

18

Location

Switzerland

Related Subject Headings

  • p38 Mitogen-Activated Protein Kinases
  • Zonula Occludens-1 Protein
  • Tight Junctions
  • Pulmonary Edema
  • Occludin
  • Mice
  • Humans
  • Hand, Foot and Mouth Disease
  • Endothelial Cells
  • Disease Models, Animal
 

Citation

APA
Chicago
ICMJE
MLA
NLM
Ji, W., Hu, Q., Zhang, M., Zhang, C., Chen, C., Yan, Y., … Duan, G. (2021). The Disruption of the Endothelial Barrier Contributes to Acute Lung Injury Induced by Coxsackievirus A2 Infection in Mice. Int J Mol Sci, 22(18). https://doi.org/10.3390/ijms22189895
Ji, Wangquan, Qiang Hu, Mengdi Zhang, Chuwen Zhang, Chen Chen, Yujie Yan, Xue Zhang, et al. “The Disruption of the Endothelial Barrier Contributes to Acute Lung Injury Induced by Coxsackievirus A2 Infection in Mice.Int J Mol Sci 22, no. 18 (September 13, 2021). https://doi.org/10.3390/ijms22189895.
Ji W, Hu Q, Zhang M, Zhang C, Chen C, Yan Y, et al. The Disruption of the Endothelial Barrier Contributes to Acute Lung Injury Induced by Coxsackievirus A2 Infection in Mice. Int J Mol Sci. 2021 Sep 13;22(18).
Ji, Wangquan, et al. “The Disruption of the Endothelial Barrier Contributes to Acute Lung Injury Induced by Coxsackievirus A2 Infection in Mice.Int J Mol Sci, vol. 22, no. 18, Sept. 2021. Pubmed, doi:10.3390/ijms22189895.
Ji W, Hu Q, Zhang M, Zhang C, Chen C, Yan Y, Zhang X, Chen S, Tao L, Zhang W, Jin Y, Duan G. The Disruption of the Endothelial Barrier Contributes to Acute Lung Injury Induced by Coxsackievirus A2 Infection in Mice. Int J Mol Sci. 2021 Sep 13;22(18).

Published In

Int J Mol Sci

DOI

EISSN

1422-0067

Publication Date

September 13, 2021

Volume

22

Issue

18

Location

Switzerland

Related Subject Headings

  • p38 Mitogen-Activated Protein Kinases
  • Zonula Occludens-1 Protein
  • Tight Junctions
  • Pulmonary Edema
  • Occludin
  • Mice
  • Humans
  • Hand, Foot and Mouth Disease
  • Endothelial Cells
  • Disease Models, Animal