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Updated: Jun 3, 2026
Intravital Microscopy of Leukocyte-endothelial and Platelet-leukocyte Interactions in Mesenterial Veins in Mice
Published on: August 13, 2015
P-selectin mediates the microvascular dysfunction associated with persistent cytomegalovirus infection in
Evgeny Senchenkov1, Mikhail V Khoretonenko, Igor L Leskov
1Department of Molecular and Cellular Physiology Center for Molecular and Tumor Virology Department of Medicine, Louisiana State University Health Sciences Center, Shreveport, Louisiana, USA.
Objective:
Cytomegalovirus has been implicated in cardiovascular disease, possibly through the induction of inflammatory processes. P-selectin and L-selectin are adhesion molecules that mediate early microvascular responses to inflammatory stimuli. This study examined the role of these selectins in the microvascular dysfunction that occurs during persistent CMV infection.
Methods:
C57Bl/6, P- or L-selectin-deficient mice were mock-inoculated or infected with murine CMV, and five weeks later placed on normal diet or high cholesterol diet for six weeks. P-selectin expression was measured or intravital microscopy was performed to determine arteriolar vasodilation and venular blood cell recruitment.
Results:
P-selectin expression was significantly increased in the heart, lung, and spleen of mCMV-ND, but not mCMV-HC C57Bl/6. mCMV-ND and mCMV-HC exhibited impaired arteriolar function, which was reversed by treatment with an anti-P-selectin antibody, but not L-selectin deficiency. mCMV-HC also showed elevated leukocyte and platelet recruitment. P-selectin inhibition abrogated, whereas L-selectin deficiency partially reduced these responses.
Conclusions:
We provide the first evidence for P-selectin upregulation by persistent mCMV infection and implicate this adhesion molecule in the associated arteriolar dysfunction. P-selectin, and to a lesser extent L-selectin, mediates the leukocyte and platelet recruitment induced by CMV infection combined with hypercholesterolemia.
Insights
Persistent cytomegalovirus (CMV) infection upregulates P-selectin, contributing to cardiovascular microvascular dysfunction. P-selectin inhibition reversed arteriolar dysfunction, highlighting its role in CMV-induced inflammation.
Area of Science:
- Immunology
- Cardiovascular Biology
- Infectious Diseases
Background:
- Cytomegalovirus (CMV) infection is linked to cardiovascular disease.
- P-selectin and L-selectin are key adhesion molecules in inflammatory responses.
Purpose of the Study:
- To investigate the role of P-selectin and L-selectin in microvascular dysfunction during persistent CMV infection.
Main Methods:
- Murine cytomegalovirus (mCMV) infection in wild-type and selectin-deficient mice.
- Dietary interventions (normal vs. high cholesterol).
- Assessment of arteriolar vasodilation and leukocyte/platelet recruitment via intravital microscopy.
Main Results:
- P-selectin expression increased in mCMV-infected mice.
- Impaired arteriolar function in mCMV infection was reversed by anti-P-selectin antibody.
- P-selectin inhibition significantly reduced leukocyte and platelet recruitment.
Conclusions:
- Persistent CMV infection upregulates P-selectin, contributing to arteriolar dysfunction.
- P-selectin plays a critical role in CMV-induced inflammation and microvascular changes, especially with hypercholesterolemia.
Related Concept Videos
01:25Selectins
01:27Cytomegalovirus Disease