The effect of herpesvirus infection on the expression of cell adhesion molecules on cultured human dermal microvascular endothelial cells

Kim, You Chan; Bang, Dongsik; Lee, Sungnack; Lee, Kwang Hoon

doi:10.1016/s0923-1811(00)00080-3

Cited by 22 publications

(22 citation statements)

References 20 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…The kinetics of E-selectin, ICAM-1 and VCAM-1 expression that we observed are consistent with previous observations facilitated by HDMEC (Heckmann and Pirthauer, 1998;Kim et al, 2000;Asahina et al, 2001).…”

Section: Discussionsupporting

confidence: 93%

Effects of antioxidants and nitric oxide on TNF-α-induced adhesion molecule expression and NF-κB activation in human dermal microvascular endothelial cells

et al. 2004

View full text Add to dashboard Cite

Section: Discussionsupporting

confidence: 93%

Effects of antioxidants and nitric oxide on TNF-α-induced adhesion molecule expression and NF-κB activation in human dermal microvascular endothelial cells

et al. 2004

View full text Add to dashboard Cite

“…Endothelial CAMs such as immunoglobulin superfamily members (intracellular adhesion moleulce, ICAM-1; vascular cell adhesion protein, VCAM-1) and selectins interact with their leukocyte integrins counterparts (very late antigen 4, VLA-4; and lymphocyte function-associated antigen1, LFA-1) and, in concert with chemotactic chemokines, facilitate rolling and adhesion of leukocytes on the endothelial wall. Under healthy conditions the endothelial cells of the BBB express very low levels of CAMs, however the expression of multiple CAMs including ICAM-1, VCAM-1, and selectins upon inflammatory stimulation multiple sclerosis (MS) [12] or infection with viruses such as human immunodeficiency virus (HIV) [13], [14] and herpes simplex virus [15].…”

Section: Introductionmentioning

confidence: 99%

West Nile Virus-Induced Cell Adhesion Molecules on Human Brain Microvascular Endothelial Cells Regulate Leukocyte Adhesion and Modulate Permeability of the In Vitro Blood-Brain Barrier Model

2014

View full text Add to dashboard Cite

Characterizing the mechanisms by which West Nile virus (WNV) causes blood-brain barrier (BBB) disruption, leukocyte infiltration into the brain and neuroinflammation is important to understand the pathogenesis of WNV encephalitis. Here, we examined the role of endothelial cell adhesion molecules (CAMs) in mediating the adhesion and transendothelial migration of leukocytes across human brain microvascular endothelial cells (HBMVE). Infection with WNV (NY99 strain) significantly induced ICAM-1, VCAM-1, and E-selectin in human endothelial cells and infected mice brain, although the levels of their ligands on leukocytes (VLA-4, LFA-1and MAC-1) did not alter. The permeability of the in vitro BBB model increased dramatically following the transmigration of monocytes and lymphocytes across the models infected with WNV, which was reversed in the presence of a cocktail of blocking antibodies against ICAM-1, VCAM-1, and E-selectin. Further, WNV infection of HBMVE significantly increased leukocyte adhesion to the HBMVE monolayer and transmigration across the infected BBB model. The blockade of these CAMs reduced the adhesion and transmigration of leukocytes across the infected BBB model. Further, comparison of infection with highly neuroinvasive NY99 and non-lethal (Eg101) strain of WNV demonstrated similar level of virus replication and fold-increase of CAMs in HBMVE cells suggesting that the non-neuropathogenic response of Eg101 is not because of its inability to infect HBMVE cells. Collectively, these results suggest that increased expression of specific CAMs is a pathological event associated with WNV infection and may contribute to leukocyte infiltration and BBB disruption in vivo. Our data further implicate that strategies to block CAMs to reduce BBB disruption may limit neuroinflammation and virus-CNS entry via ‘Trojan horse’ route, and improve WNV disease outcome.

show abstract

“…5). Enhancement of endothelial cell E-selection expression by patients' serum and increased inflammatory cell binding to endothelial cells in the presence of infectious agents have also been detected [67,68].…”

Section: Endothelial Cellsmentioning

confidence: 95%

Pathogenesis of Adamantiades-Beh�et's disease

Zouboulis

May

2003

Medical Microbiology and Immunology

View full text Add to dashboard Cite

The aetiology of Adamantiades-Behçet's disease remains unknown and its pathogenesis is not fully understood. Linked intrinsic and extrinsic factors are thought to contribute to the development of the disease, which probably occurs by environmental triggering of a genetically determined disorder. Transmission is solely vertical, indicating that the disease is not contagious. Genetic factors have been investigated and a significant link of HLA-B51, especially of HLA-B5101, has been identified. However, none of the functional correlates of the disease appear to be restricted by HLA-B51. Recently, the role of the genes encoding TNF, Tap proteins and MICA has been emphasised. Extrinsic pathogenetic candidates have been identified, including bacterial ( Streptococcus sanguis, Mycoplasma fermentas) and viral (human herpes virus) antigens and environmental pollution, which may cross-react with oral mucosal antigens and induce immunological mechanisms. A common factor linking some of the possible pathogenetic agents is extrinsically induced tissue stress or heat shock proteins, which react with host tissues and elicit significant Th1 cell responses. Neutrophils may also play a role in the pathogenesis of the disease, as they are attracted by macrophages and activated endothelial cells, which release cytokines and chemokines (especially IL-8) at the site of the lesions, and thus contribute to tissue damage and self maintenance of inflammation. Endothelial activation leading to a chronic local inflammation process together with platelet and serum factors enhance coagulation and thrombosis.

show abstract

The effect of herpesvirus infection on the expression of cell adhesion molecules on cultured human dermal microvascular endothelial cells

Cited by 22 publications

References 20 publications

Effects of antioxidants and nitric oxide on TNF-α-induced adhesion molecule expression and NF-κB activation in human dermal microvascular endothelial cells

Effects of antioxidants and nitric oxide on TNF-α-induced adhesion molecule expression and NF-κB activation in human dermal microvascular endothelial cells

West Nile Virus-Induced Cell Adhesion Molecules on Human Brain Microvascular Endothelial Cells Regulate Leukocyte Adhesion and Modulate Permeability of the In Vitro Blood-Brain Barrier Model

Pathogenesis of Adamantiades-Beh�et's disease

Contact Info

Product

Resources

About