Abstract
Objective: We investigated the in vitro effects of low- and high-dose methylprednisolone (MP) on the cytokine-induced expression of HLA-DR, ICAM-1 and VCAM-1 on human brain microvessel endothelial cells (HBMECs). Methods: Brain endothelium was obtained from microvessels included in the apparently normal white matter of surgical specimens of nine patients. Cells were stained with monoclonal antibodies anti-HLA-DR, anti-ICAM-1 and anti-VCAM-1 and analysed by flow cytometry as fluorescence histograms. The mean fluorescence intensity (MFI) of HBMECs treated with different stimuli was calculated. Results: γ-IFN-induced HLA-DR was down-regulated in a dose-dependent manner by MP. High-dose MP reduced the TNF-α-induced ICAM-1 and VCAM-1 expression. Conclusions: The down-regulation of adhesion molecules on cerebral endothelial cells could decrease mononuclear cell transmigration through the blood brain barrier and consequently the perivascular infiltrates. The results add support to the rationale for high-dose MP treatment in multiple sclerosis relapses.
| Original language | English |
|---|---|
| Pages (from-to) | 241-244 |
| Number of pages | 4 |
| Journal | Canadian Journal of Neurological Sciences |
| Volume | 27 |
| Issue number | 3 |
| Publication status | Published - 2000 |
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ASJC Scopus subject areas
- Clinical Neurology
- Neuroscience(all)
Cite this
High-dose methylprednisolone reduces cytokine-induced adhesion molecules on human brain endothelium. / Gelati, M.; Corsini, E.; Dufour, A.; Massa, G.; Giombini, S.; Solero, C. L.; Salmaggi, A.
In: Canadian Journal of Neurological Sciences, Vol. 27, No. 3, 2000, p. 241-244.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - High-dose methylprednisolone reduces cytokine-induced adhesion molecules on human brain endothelium
AU - Gelati, M.
AU - Corsini, E.
AU - Dufour, A.
AU - Massa, G.
AU - Giombini, S.
AU - Solero, C. L.
AU - Salmaggi, A.
PY - 2000
Y1 - 2000
N2 - Objective: We investigated the in vitro effects of low- and high-dose methylprednisolone (MP) on the cytokine-induced expression of HLA-DR, ICAM-1 and VCAM-1 on human brain microvessel endothelial cells (HBMECs). Methods: Brain endothelium was obtained from microvessels included in the apparently normal white matter of surgical specimens of nine patients. Cells were stained with monoclonal antibodies anti-HLA-DR, anti-ICAM-1 and anti-VCAM-1 and analysed by flow cytometry as fluorescence histograms. The mean fluorescence intensity (MFI) of HBMECs treated with different stimuli was calculated. Results: γ-IFN-induced HLA-DR was down-regulated in a dose-dependent manner by MP. High-dose MP reduced the TNF-α-induced ICAM-1 and VCAM-1 expression. Conclusions: The down-regulation of adhesion molecules on cerebral endothelial cells could decrease mononuclear cell transmigration through the blood brain barrier and consequently the perivascular infiltrates. The results add support to the rationale for high-dose MP treatment in multiple sclerosis relapses.
AB - Objective: We investigated the in vitro effects of low- and high-dose methylprednisolone (MP) on the cytokine-induced expression of HLA-DR, ICAM-1 and VCAM-1 on human brain microvessel endothelial cells (HBMECs). Methods: Brain endothelium was obtained from microvessels included in the apparently normal white matter of surgical specimens of nine patients. Cells were stained with monoclonal antibodies anti-HLA-DR, anti-ICAM-1 and anti-VCAM-1 and analysed by flow cytometry as fluorescence histograms. The mean fluorescence intensity (MFI) of HBMECs treated with different stimuli was calculated. Results: γ-IFN-induced HLA-DR was down-regulated in a dose-dependent manner by MP. High-dose MP reduced the TNF-α-induced ICAM-1 and VCAM-1 expression. Conclusions: The down-regulation of adhesion molecules on cerebral endothelial cells could decrease mononuclear cell transmigration through the blood brain barrier and consequently the perivascular infiltrates. The results add support to the rationale for high-dose MP treatment in multiple sclerosis relapses.
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M3 - Article
VL - 27
SP - 241
EP - 244
JO - Canadian Journal of Neurological Sciences
JF - Canadian Journal of Neurological Sciences
SN - 0317-1671
IS - 3
ER -