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Increased expression of adhesion molecules (CD54, CD29 and CD44) on fibroblasts infected with cytomegalovirus
1Department of Pediatrics, Mie University School of Medicine, Japan.
Abstract:
The expression of ICAM-1 (CD54), beta 1 integrin (CD29), and CD44 on cytomegalovirus (CMV)-infected human embryonic fibroblasts (HEF) was analyzed by flow cytometry. The expression of these adhesion molecules increased significantly on CMV-infected HEF, on days 2 and 5 after inoculation, compared to uninfected HEF. However, the expression of these adhesion molecules decreased on herpes simplex virus (HSV)-1 and varicella-zoster virus (VZV)-infected HEF. Increased expression was not observed on HEF treated either with inactivated CMV or with supernatant fluid of CMV-infected cells. The addition of anti-cytokine (TNF-alpha, IL-1 beta, or IFN-gamma) antibodies had no effect on the increase of these adhesion molecules. This suggests that the increase in CD54, CD29, and CD44 on CMV-infected cells requires active virus replication and was not mediated by a soluble factor released from CMV-infected cells. Changes in adhesion molecules on CMV-infected fibroblasts may contribute to inflammation induced by CMV infection.
Insights
Cytomegalovirus (CMV) infection increases adhesion molecules like ICAM-1 (CD54) on human embryonic fibroblasts (HEF). This viral effect, requiring active replication, may contribute to CMV-induced inflammation.
Area of Science:
- Virology
- Immunology
- Cell Biology
Background:
- Adhesion molecules play crucial roles in cell-cell interactions and immune responses.
- Cytomegalovirus (CMV) is a common human pathogen with significant clinical implications.
- Understanding how viral infections alter host cell surface molecules is vital for comprehending pathogenesis.
Purpose of the Study:
- To investigate the expression of specific adhesion molecules (ICAM-1/CD54, beta 1 integrin/CD29, CD44) on human embryonic fibroblasts (HEF) following cytomegalovirus (CMV) infection.
- To differentiate the effects of active CMV infection from inactivated virus or soluble factors.
- To explore the potential role of cytokines in modulating adhesion molecule expression during CMV infection.
Main Methods:
- Flow cytometry was employed to quantify the expression levels of ICAM-1 (CD54), beta 1 integrin (CD29), and CD44.
- Human embryonic fibroblasts (HEF) were infected with cytomegalovirus (CMV), herpes simplex virus (HSV)-1, and varicella-zoster virus (VZV).
- HEF were also treated with inactivated CMV and CMV-infected cell supernatant, and cytokine-neutralizing antibodies were used.
Main Results:
- CMV infection significantly upregulated ICAM-1 (CD54), beta 1 integrin (CD29), and CD44 expression on HEF at days 2 and 5 post-inoculation.
- In contrast, HSV-1 and VZV infections led to decreased expression of these adhesion molecules.
- Increased adhesion molecule expression was dependent on active CMV replication and not mediated by soluble factors or cytokines (TNF-alpha, IL-1 beta, IFN-gamma).
Conclusions:
- Active CMV replication, but not other herpesviruses like HSV-1 or VZV, upregulates key adhesion molecules on human embryonic fibroblasts.
- The observed increase in CD54, CD29, and CD44 expression is virus-driven and independent of soluble mediators or common inflammatory cytokines.
- These alterations in adhesion molecule expression during CMV infection may play a role in the inflammatory processes associated with CMV disease.