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 Research: Interferon Beta 1b (Betaseron) Might Work by Plugging the Blood-Brain Barrier

Blood-Brain Barrier (BBB)

Very interesting new research that shows that Inteferon beta 1b (available in Betaseron) might work by preventing leukocytes (white blood cells) from crossing the blood brain barrier.

"Adhesion molecules (AMs) are believed to regulate the transmigration of blood leukocytes across the blood-brain barrier (BBB), which is an essential step in the pathogenesis of multiple sclerosis (MS)...

The expression levels of cell surface bound AMs on blood MNC remained stable during treatment. Untreated MS patients, however, showed a continuous decrease in the expression of cell surface bound AM expression over 18 months. Stabilisation of the expression of cell surface bound AMs on blood MNC may indicate the beneficial effects of IFN-beta(1b) therapy in MS patients."

PMID: 15083294 [PubMed - in process]

Click "read more" for the full abstract...

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Full Article Text

Interferon-beta(1b) leads to a short-term increase of soluble but long-term stabilisation of cell surface bound adhesion molecules in multiple sclerosis.

Kraus J, Bauer R, Chatzimanolis N, Engelhardt B, Tofighi J, Bregenzer T, Kuehne BS, Stolz E, Blaes F, Morgen K, Traupe H, Kaps M, Oschmann P.


Justus-Liebig University of Giessen, Dept. of Neurology, 35385, Giessen, Germany, joerg.kraus@ukmuenster.de

Adhesion molecules (AMs) are believed to regulate the transmigration of blood leukocytes across the blood-brain barrier (BBB), which is an essential step in the pathogenesis of multiple sclerosis (MS). Previous studies have investigated changes of the soluble forms of AM during interferon-beta(1b) (IFN-beta(1b)) treatment in MS patients. In this study, we analysed the influence of IFN-beta(1b) treatment on the cell surface bound forms of the AMs cICAM-1 and cICAM-3 on blood mononuclear cells (MNC). Sixty-eight patients with relapsing-remitting MS were enrolled in this open study; thirty of them were treated with IFN-beta(1b). Blood samples were collected every three months over a period of 18 months. The expression levels of cell surface bound forms of AM on blood MNC were measured by two colour flow cytometry analysis. sVCAM-1, sICAM-1 and sICAM-3 were determined by ELISA. We found a short-term induction effect on the serum concentrations of sICAM-1 and sVCAM-1 after three months of IFN-beta(1b) treatment. The expression levels of cell surface bound AMs on blood MNC remained stable during treatment. Untreated MS patients, however, showed a continuous decrease in the expression of cell surface bound AM expression over 18 months. Stabilisation of the expression of cell surface bound AMs on blood MNC may indicate the beneficial effects of IFN-beta(1b) therapy in MS patients.

PMID: 15083294 [PubMed - in process]

Original article can be found here




 
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