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Open AccessArticle

The S100B Inhibitor Pentamidine Ameliorates Clinical Score and Neuropathology of Relapsing—Remitting Multiple Sclerosis Mouse Model

1
Department of Translational Medicine and Surgery, Section of General Pathology, Università Cattolica del Sacro Cuore, Largo Francesco Vito 1, 00168 Rome, Italy
2
Fondazione Policlinico Universitario A. Gemelli IRCCS, Largo Agostino Gemelli 1-8, 00168 Rome, Italy
3
Cellular Neurobiology Unit, Preclinical Neuroscience, IRCCS Santa Lucia Foundation, Via del Fosso di Fiorano 65, 00143 Rome, Italy
4
Istituto di Scienze e Tecnologie Chimiche “Giulio Natta” SCITEC-CNR, Largo Francesco Vito 1, 00168 Rome, Italy
5
Institute for Systems Analysis and Computer Science, IASI-CNR, Largo Francesco Vito 1, 00168 Rome, Italy
6
Department of Neuroscience, Università Cattolica del Sacro Cuore, Largo Francesco Vito 1, 00168 Rome, Italy
7
IRCCS San Raffaele Scientific Institute, Università Vita-Salute San Raffaele, 20132 Milan, Italy
*
Authors to whom correspondence should be addressed.
Equally contributed as second authors.
Cells 2020, 9(3), 748; https://doi.org/10.3390/cells9030748
Received: 24 February 2020 / Revised: 16 March 2020 / Accepted: 17 March 2020 / Published: 18 March 2020
S100B is an astrocytic protein acting either as an intracellular regulator or an extracellular signaling molecule. A direct correlation between increased amount of S100B and demyelination and inflammatory processes has been demonstrated. The aim of this study is to investigate the possible role of a small molecule able to bind and inhibit S100B, pentamidine, in the modulation of disease progression in the relapsing–remitting experimental autoimmune encephalomyelitis mouse model of multiple sclerosis. By the daily evaluation of clinical scores and neuropathologic-molecular analysis performed in the central nervous system, we observed that pentamidine is able to delay the acute phase of the disease and to inhibit remission, resulting in an amelioration of clinical score when compared with untreated relapsing–remitting experimental autoimmune encephalomyelitis mice. Moreover, we observed a significant reduction of proinflammatory cytokines expression levels in the brains of treated versus untreated mice, in addition to a reduction of nitric oxide synthase activity. Immunohistochemistry confirmed that the inhibition of S100B was able to modify the neuropathology of the disease, reducing immune infiltrates and partially protecting the brain from the damage. Overall, our results indicate that pentamidine targeting the S100B protein is a novel potential drug to be considered for multiple sclerosis treatment. View Full-Text
Keywords: S100B; multiple sclerosis; relapsing–remitting experimental autoimmune encephalomyelitis; pentamidine S100B; multiple sclerosis; relapsing–remitting experimental autoimmune encephalomyelitis; pentamidine
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Di Sante, G.; Amadio, S.; Sampaolese, B.; Clementi, M.E.; Valentini, M.; Volonté, C.; Casalbore, P.; Ria, F.; Michetti, F. The S100B Inhibitor Pentamidine Ameliorates Clinical Score and Neuropathology of Relapsing—Remitting Multiple Sclerosis Mouse Model. Cells 2020, 9, 748.

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