PMID- 15072749
OWN - NLM
STAT- MEDLINE
DCOM- 20040805
LR  - 20061115
IS  - 1386-6532 (Print)
IS  - 1386-6532 (Linking)
VI  - 30
IP  - 1
DP  - 2004 May
TI  - Towards an in vitro model for acute hemorrhagic conjunctivitis: cytokine-mediated 
      vascular endothelial cell activation triggered by enterovirus type 70 infection.
PG  - 19-23
AB  - BACKGROUND: Little is known of the pathogenetic mechanisms of enterovirus type 70 
      (EV70), a causative agent of acute hemorrhagic conjunctivitis. However, virus- or 
      cytokine-induced perturbation of vascular endothelial cells are potential 
      triggering events. OBJECTIVE: To determine whether EV70 infection of human 
      umbilical vascular endothelial cells (HUVECs) and human corneal epithelial cells 
      (HCEs) causes the release of vasoactive cytokines, capable of triggering vascular 
      endothelial cell activation. STUDY DESIGN: Susceptibility of cultured HUVECs and 
      HCEs to EV70 was tested by observing the appearance of cytopathic effect or 
      immunoprecipitation of viral protein in infected cells. The culture fluids from 
      the virus-infected cells were tested for their ability to stimulate the 
      expression of intercellular adhesion molecule-1 (ICAM-1) on uninfected HUVECs. 
      Anti-cytokine antibodies were used to identify ICAM-1-activating cytokine(s). 
      RESULTS: Both HUVECs and HCEs were susceptible to EV70 infection. Culture fluids 
      from EV70-infected HUVECs and HCEs stimulated ICAM-l expression on uninfected 
      HUVECs, which was completely blocked by anti-interleukin-1alpha (IL-1alpha) 
      antibody but not by interleukin-1beta (IL-1beta) or anti-tumor necrosis factor 
      alpha (TNFalpha) antibodies. CONCLUSION: This study provides the first evidence 
      of EV70 infection of both HCEs and HUVECs, and furthermore, identifies IL-1alpha 
      as the predominant endothelial cell-activating factor produced by EV70-infected 
      cells. Since endothelial cell activation is often an initiating step towards 
      vascular permeability and/or inflammation, the perturbation of endothelial cell 
      function through EV70 induced IL-1alpha is thus a potential contributory factor 
      in the pathogenesis of EV70-associated hemorrhagic conjunctivitis.
FAU - Chang, Cheng-Hsien
AU  - Chang CH
AD  - Department of Ophthalmology, Kaohsiung Medical University, Kaohsiung, Taiwan.
FAU - Lin, Kuei-Hsiang
AU  - Lin KH
FAU - Anderson, Robert
AU  - Anderson R
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - Netherlands
TA  - J Clin Virol
JT  - Journal of clinical virology : the official publication of the Pan American 
      Society for Clinical Virology
JID - 9815671
RN  - 0 (Antibodies)
RN  - 0 (Interleukin-1)
RN  - 0 (Tumor Necrosis Factor-alpha)
RN  - 126547-89-5 (Intercellular Adhesion Molecule-1)
SB  - IM
MH  - Antibodies
MH  - Capillary Permeability
MH  - Cells, Cultured
MH  - Conjunctivitis, Acute Hemorrhagic/immunology/*virology
MH  - Cytopathogenic Effect, Viral
MH  - Endothelial Cells/*immunology/*virology
MH  - Enterovirus D, Human/growth & development/*pathogenicity
MH  - Epithelial Cells/immunology/virology
MH  - Epithelium, Corneal/immunology/*virology
MH  - Gene Expression Regulation
MH  - Humans
MH  - Intercellular Adhesion Molecule-1/biosynthesis
MH  - Interleukin-1/*immunology/metabolism
MH  - Tumor Necrosis Factor-alpha/immunology
EDAT- 2004/04/10 05:00
MHDA- 2004/08/06 05:00
CRDT- 2004/04/10 05:00
PHST- 2003/03/31 00:00 [received]
PHST- 2003/07/01 00:00 [revised]
PHST- 2003/07/29 00:00 [accepted]
PHST- 2004/04/10 05:00 [pubmed]
PHST- 2004/08/06 05:00 [medline]
PHST- 2004/04/10 05:00 [entrez]
AID - S1386653203002294 [pii]
AID - 10.1016/j.jcv.2003.07.003 [doi]
PST - ppublish
SO  - J Clin Virol. 2004 May;30(1):19-23. doi: 10.1016/j.jcv.2003.07.003.