International Journal of Immunopharmacology
Research paperInhibition of blood-brain barrier disruption in experimental allergic encephalomyelitis by short-term therapy with dexamethasone or cyclosporin A
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2021, Pharmacology and TherapeuticsCitation Excerpt :IL-1β is a key pro-inflammatory cytokine mediating the neuroinflammation to promote innate immune response during the pathological procession in CNS-related diseases, including MS (Lalor et al., 2011). In the EAE or MS progressing event, a characteristic is BBB and BSCB leakage, immune cell infiltration into CSF and CNS, which leads to release of IL-1β and drive neuroinflammation (Alvarez et al., 2011; Barclay & Shinohara, 2017; Dendrou et al., 2015; Kermode et al., 1990; Paul & Bolton, 1995). This was verified by being detected the IL-1β in EAE rats or blood of MS patients.
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2017, Experimental ParasitologyCitation Excerpt :In the present study, the higher activity of MMP-2 and -9 in AR raises the possibility that ABZ treatment enhances the disease pathogenesis through enhanced MMP-2 and MMP-9 activities. Earlier study on experimental allergic encephalomyelitis showed that steroid treatment inhibited the BBB disruption (Paul and Bolton, 1995). It was also found that steroid treatment reduced the expression of MMP-9 in CNS vascular endothelium (Harkness et al., 2000).
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2014, Journal of NeuroimmunologyCitation Excerpt :After IV-MP treatment for relapse in MSR patients, we observed an increment on the proportion of circulating total CD19+ B-cells, as in other authors (Krystyna et al., 2009), while decreased proportions of CD3+ T lymphocytes (data not shown) as in our previous study (Navarro et al., 2006). Following IV-MP treatment, a reduced amount of soluble VCAM-1 and E-selectin in the serum of MS patients has been shown (Elovaara et al., 2000) that could reduce the migration of these cells into CNS, as glucocorticoids inhibit the disruption of the BBB and thereby reduce leukocyte infiltration into the CNS (Paul and Bolton, 1995). We also observed a decrease in the proportion on the regulatory CD19+CD25+FoxP+ and CD19+FoxP+ after IV-MP.
C16 peptide shown to prevent leukocyte infiltration and alleviate detrimental inflammation in acute allergic encephalomyelitis model
2013, NeuropharmacologyCitation Excerpt :The inflammatory reaction in the CNS is driven by activated auto-reactive immune cells penetrating the CNS and damaging myelin antigens (Kent et al., 1995). The vulnerability of the CNS and the progression of deficits from caudal to rostral have been attributed to the increased permeability of the blood brain barrier (BBB) and activated macrophage or microglia mediated demyelination (Claudio et al., 1989; Paul and Bolton, 1995; Yin et al., 2010). In CNS inflammation, the up-regulation of surface cell adhesion molecules in peripheral blood cells is a prerequisite for their interaction with activated ependymal and endothelial cells, and their crossing of the blood–brain barrier (Schenkel et al., 2004).
Animal models of multiple sclerosis-Potentials and limitations
2010, Progress in NeurobiologyCitation Excerpt :the phosphodiesterase-4 inhibitor rolipram, while very effective in suppressing EAE, failed to suppress inflammatory activity as gleaned through magnetic resonance imaging in a pilot trial in patients with relapsing–remitting MS (Bielekova et al., 2009), the immunosuppressive drug cyclosporin A prevented BBB disruption and suppressed the development of EAE, but was classified as unacceptable for treatment of MS based on risk/benefit consideration due to low efficacy and frequent adverse reactions (Goodin et al., 2002; Kappos et al., 1988; Kieseier and Hartung, 2003; McCombe et al., 1999; Paul and Bolton, 1995). If one therefore considers only the therapeutic trials conducted in EAE and their translation into the clinic, it may well be regarded as a misleading model of MS. However, several aspects of the aetiopathogenesis of MS such as susceptibility genes, immunoregulatory circuits, mechanisms of immune cell activation, migration and elimination as well as of nervous tissue destruction and repair have been successfully studied in EAE rendering it a useful model of MS (Hemmer and Hartung, 2007; Schreiner et al., 2009).