Magnetic brain stimulation upregulates adhesion and prevents EAE: MMP-2, ICAM-1, and VCAM-1 in the choroid plexus as a target

We are most thankful to Prof. Yehuda Shoenfeld, head of Autoimmunity Center, Sheba Hospital at Tel Aviv, University in Israel, for critical and constructive comments on the manuscript. Thanks to Prof. B. Reljin and N. Stepanic, School of Informational Technology, Universirty of Belgrade for contribution in molecular images and computing analysis. Authors gratefully acknowledge the repeated gifts of the magnetic beads for magnetic brain stimulation of rats presented by Institute for Nuclear Physics, Vincha, Belgrade. Clinical signs appearance and significant increases of ICAM-1 and MMP-2 expressions with the clusters of VCAM-1(+) immunoreactivity in the choroids plexus epithelium to transferred anti-myelin oligodendroglial antibodies into the third brain ventricle, indicate important role of choroids plexus in the induction of acute experimental autoimmune encephalomyelitis (EAE). Magnetic brain stimulation with AKMA micro-magnet flux density of 60 miliTesla, 5 mm in diameter, implanted upon the pineal gland (PG), immediately after antibody injection, significantly decreases the expression of MMP-2 and ICAM-1 in the choroids plexus of the rat brain and abruptly suppresses the induction of acute EAE

Autoimmunity in the brain: The pathogenesis insight from cell biology

The aim of the study is to explore the relationship between leakage of the blood-brain barrier and inflammation, the reason why demyelination occurs - seemingly in the absence of an antigen-specific immune response that requires explanation if a coherent account of an inflammatory-mediated demyelination is to be achieved. In this study the cellular biology of the glial cells important for the synthesis and maintenance of central nervous system (CNS) myelin and their inter-relations with other environmental cells (neuronal, microglial, olygodendroglial, astrocytes, endothelial, epithelial, T lymphocytes, B lymphocytes, monocytes, and macrophages) and with the compound of the extracellular matrix (ECM) during the development of an autoimmune inflammatory and demyelinating processes in the brain was analyzed. Upon activation in the peripheral tissue, immune cells reach their target organ via bloodstream and interacting with blood vessels wall components in the absence of exogenous stimulus mount an attack against the local milleu, which is the starting point of a pathogenic inflammatory reaction. Each of these contacts may trigger profuse secretion of cytokines, chemokines, and other soluble inflammatory mediators, which in the CNS by activating of local glial cells and by attracting and stimulating blood-borne monocyte/macrophages can act directly on neural cells and will cause their demyelination