Measles virus hemagglutinin mediates monocyte aggregation and increased adherence to measles-infected endothelial cells

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• 作者：M. Soilu-H?nninen ; Arno H?nninen ; Jorma Ilonen ; Aimo Salmi and R. Salonen
• 关键词：Key words Measles virus ; Leukocyte integrins ; Adhesion ; Vascular endothelium
• 刊名：Medical Microbiology and Immunology
• 出版年：1996
• 出版时间：September 1996
• 年：1996
• 卷：185
• 期：2
• 页码：73-80
• 全文大小：721 KB
• 刊物类别：Biomedical and Life Sciences
• 刊物主题：Biomedicine
  Medical Microbiology
  Immunology
  
• 出版者：Springer Berlin / Heidelberg
• ISSN：1432-1831

文摘

The effect of measles virus (MV) infection on monocyte adhesion was studied using human peripheral blood monocytes and monocytic and endothelial cell lines. The infection of monocytic U-937 cells led to the formation of large cellular aggregates. Aggregation was independent of intercellular adhesion molecule-1 (ICAM-1)/ lymphocyte function-associated antigen-1 (LFA-1), but could be inhibited by monoclonal antibodies (mAb) against the MV hemagglutinin glycoprotein (MV-H). mAb against the MV receptor, CD46, also blocked aggregation. No significant changes in the cell surface expression of adhesion molecules CD11a, CD11b, CD11c, CD18, CD54, CD44, CD49d (α4-integrin) and CD62L (L-selectin) were observed on MV-infected monocytes. Infection of a human endothelial cell line, EAhy 926 (HEC), with MV led to a two-fold increase in ICAM-1 expression and a two-fold increase in monocyte adherence to the HEC (from 22±1.6% to 42±4.8%). However, ICAM-1 mAb reduced monocyte adhesion to the control and MV-infected HEC to a similar degree, whereas anti-MV-H antibodies abolished the difference between binding to infected and control HEC. We conclude that MV hemagglutinin mediated both the homotypic aggregation in infected monocyte cultures and increased monocyte adherence to the infected endothelial cells.