Interleukin-1α released from epithelial cells after adenovirus type 37 infection activates intercellular adhesion molecule 1 expression on human vascular endothelial cells

被引:19
作者
Chang, CH
Huang, Y
Issekutz, AC
Griffith, M
Lin, KH
Anderson, R [1 ]
机构
[1] Dalhousie Univ, Dept Microbiol & Immunol, Halifax, NS B3H 4H7, Canada
[2] Dalhousie Univ, Dept Pathol, Halifax, NS B3H 4H7, Canada
[3] Dalhousie Univ, Dept Pediat, Halifax, NS B3H 4H7, Canada
[4] Univ Ottawa, Inst Eye, Ottawa, ON K1H 8L6, Canada
[5] Kaohsiung Med Univ, Dept Ophthalmol, Kaohsiung, Taiwan
[6] Kaohsiung Med Univ, Clin Lab, Kaohsiung, Taiwan
关键词
D O I
10.1128/JVI.76.1.427-431.2002
中图分类号
Q93 [微生物学];
学科分类号
071005 ; 100705 ;
摘要
A key event in virus-induced inflammation (leukocyte extravasation through the endothelium) is the local activation of endothelial cells, as indicated by the expression of adhesion molecules such as intercellular adhesion molecule 1 (ICAM-1), vascular cell adhesion molecule 1 (VCAM-1), and E-selectin. In order to identify triggers of inflammation in adenovirus infection, we inoculated respiratory and ocular epithelial cells with adenovirus type 37 (Ad37), a human pathogen associated with keratoconjunctivitis as well as urogenital and respiratory infections. Fluids from virus-infected epithelial cells activated ICAM-1 (and to a lesser extent, VCAM-1) expression on cultured human umbilical vein endothelial cells. Blocking studies with anticytokine antibodies implicated interleukin-1 alpha (IL-1 alpha) as the epithelial cell-derived factor which activated endothelial cell ICAM-1 expression. The results thus identify epithelial cell-derived IL-1 alpha as a potentially important activator of endothelial cells in Ad37-induced inflammation.
引用
收藏
页码:427 / 431
页数:5
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