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Cytomegalovirus induced PMN adherence in relation to an ELAM-1 antigen present on infected endothelial cell
A H Span1, W Mullers, A M Miltenburg
1Department of Medical Microbiology, University of Limburg, Maastricht, The Netherlands.
Abstract:
In human umbilical vein endothelial cells infected with cytomegalovirus (CMV), an activation antigen recognized by monoclonal antibody (mAb) ENA1 appeared. mAb ENA1 reacts with an inducible endothelial surface antigen which has characteristics similar to those of ELAM-1. Incubation with anti-IL-1 partly inhibited this appearance and, parallel to this, the virus-induced polymorphonuclear cell (PMN) adhesion was decreased. In addition, the adhesion of PMN to virus-infected endothelial cells could be reduced by F(ab)2 fragments of mAb ENA1 to almost control level. The results obtained after incubation of PMN with mAb IB4 (against CD18) suggest that the adhesion of PMN to uninfected endothelial cells is CD18 glycoprotein dependent, and virus infection up-regulates this glycoprotein-dependent mechanism. These results indicate that the virus-induced PMN adhesion is regulated by the following mechanism: virus infection of endothelial cells induces IL-1 production, and the autocrine IL-1 causes the expression of ELAM-1 on the surface of endothelial cells. In turn this activation antigen ELAM-1 binds with its putative ligand present on the PMN membrane. The virus-induced PMN adhesion occurs also through a CD18 glycoprotein-dependent mechanism.
Insights
Cytomegalovirus (CMV) infection induces an endothelial cell antigen, similar to ELAM-1, which promotes polymorphonuclear cell (PMN) adhesion. This virus-induced PMN adhesion is mediated by IL-1 and CD18 glycoprotein.
Area of Science:
- Immunology
- Virology
- Cell Biology
Background:
- Cytomegalovirus (CMV) infection can alter endothelial cell function.
- Endothelial cell activation plays a role in inflammatory responses.
- Polymorphonuclear cell (PMN) adhesion is a key event in inflammation.
Purpose of the Study:
- To investigate the mechanism of virus-induced PMN adhesion to endothelial cells.
- To identify the specific molecules involved in this adhesion process.
Main Methods:
- Human umbilical vein endothelial cells were infected with CMV.
- Monoclonal antibodies (mAbs) ENA1 and IB4 were used to detect cell surface antigens and inhibit adhesion.
- Interleukin-1 (IL-1) and its role in antigen expression were assessed.
- PMN adhesion assays were performed on infected and uninfected endothelial cells.
Main Results:
- CMV infection induced an endothelial surface antigen recognized by mAb ENA1, similar to ELAM-1.
- Anti-IL-1 partially inhibited the appearance of the ENA1 antigen and reduced PMN adhesion.
- F(ab)2 fragments of mAb ENA1 significantly reduced PMN adhesion to CMV-infected cells.
- PMN adhesion to uninfected cells was CD18 glycoprotein dependent, and CMV infection upregulated this mechanism.
Conclusions:
- CMV infection induces IL-1 production in endothelial cells, leading to ELAM-1 expression.
- ELAM-1 on endothelial cells binds to a ligand on PMNs, mediating virus-induced adhesion.
- A CD18 glycoprotein-dependent mechanism also contributes to virus-induced PMN adhesion.