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Immunol."],"abstract":"<jats:p>Voltage gated sodium (Nav) channels contribute to axonal damage following demyelination in experimental autoimmune encephalomyelitis (EAE), a rodent model of multiple sclerosis (MS). The Nav1.6 isoform has been implicated as a primary contributor in this process. However, the role of Nav1.6 in immune processes, critical to the pathology of both MS and EAE, has not been extensively studied. EAE was induced with myelin oligodendrocyte (MOG<jats:sub>35-55<\/jats:sub>) peptide in<jats:italic>Scn8a<jats:sup>dmu\/+<\/jats:sup><\/jats:italic>mice, which have reduced Nav1.6 levels.<jats:italic>Scn8a<jats:sup>dmu\/+<\/jats:sup><\/jats:italic>mice demonstrated improved motor capacity during the recovery and early chronic phases of EAE relative to wild-type animals. In the optic nerve, myeloid cell infiltration and the effects of EAE on the axonal ultrastructure were also significantly reduced in<jats:italic>Scn8a<jats:sup>dmu\/+<\/jats:sup><\/jats:italic>mice. Analysis of innate immune parameters revealed reduced plasma IL-6 levels and decreased percentages of Gr-1<jats:sup>high<\/jats:sup>\/CD11b<jats:sup>+<\/jats:sup>and Gr-1<jats:sup>int<\/jats:sup>\/CD11b<jats:sup>+<\/jats:sup>myeloid cells in the blood during the chronic phase of EAE in<jats:italic>Scn8a<jats:sup>dmu\/+<\/jats:sup><\/jats:italic>mice. Elevated levels of the anti-inflammatory cytokines IL-10, IL-13, and TGF-\u03b21 were also observed in the brains of untreated<jats:italic>Scn8a<jats:sup>dmu\/+<\/jats:sup><\/jats:italic>mice. A lipopolysaccharide (LPS) model was used to further evaluate inflammatory responses.<jats:italic>Scn8a<jats:sup>dmu\/+<\/jats:sup><\/jats:italic>mice displayed reduced inflammation in response to LPS challenge. To further evaluate if this was an immune cell-intrinsic difference or the result of changes in the immune or hormonal environment, mast cells were derived from the bone marrow of<jats:italic>Scn8a<jats:sup>dmu\/+<\/jats:sup><\/jats:italic>mice. These mast cells also produced lower levels of IL-6, in response to LPS, compared with those from wild type mice. Our results demonstrate that in addition to its recognized impact on axonal damage, Nav1.6 impacts multiple aspects of the innate inflammatory response.<\/jats:p>","DOI":"10.3389\/fimmu.2021.533423","type":"journal-article","created":{"date-parts":[[2021,3,19]],"date-time":"2021-03-19T04:46:28Z","timestamp":1616129188000},"update-policy":"https:\/\/doi.org\/10.3389\/crossmark-policy","source":"Crossref","is-referenced-by-count":13,"title":["Mice Heterozygous for the Sodium Channel Scn8a (Nav1.6) Have Reduced Inflammatory Responses During EAE and Following LPS Challenge"],"prefix":"10.3389","volume":"12","author":[{"given":"Barakat","family":"Alrashdi","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Bassel","family":"Dawod","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Sabine","family":"Tacke","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Stefanie","family":"Kuerten","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Patrice D.","family":"C\u00f4t\u00e9","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jean S.","family":"Marshall","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"1965","published-online":{"date-parts":[[2021,3,19]]},"reference":[{"key":"B1","doi-asserted-by":"publisher","DOI":"10.1038\/nrn2023","article-title":"Axonal conduction and injury in multiple sclerosis: The role of sodium channels","volume":"7","author":"Waxman","year":"2006","journal-title":"Nat Rev Neurosci"},{"key":"B2","doi-asserted-by":"crossref","DOI":"10.1007\/978-1-4419-0029-6_8","article-title":"Psychiatric Disorders, Stress, and Their Treatment Among People with Multiple Sclerosis","volume-title":"Psychological Co-morbidities of Physical Illness","author":"Mohr","year":"2011"},{"key":"B3","doi-asserted-by":"publisher","DOI":"10.1111\/j.1476-5381.2011.01302.x","article-title":"Experimental autoimmune encephalomyelitis (EAE) as a model for multiple sclerosis (MS)","volume":"164","author":"Constantinescu","year":"2011","journal-title":"Br J Pharmacol"},{"key":"B4","doi-asserted-by":"publisher","DOI":"10.4049\/jimmunol.1302171","article-title":"B Cells Promote Induction of Experimental Autoimmune Encephalomyelitis by Facilitating Reactivation of T Cells in the Central Nervous System","volume":"192","author":"Pierson","year":"2014","journal-title":"J Immunol"},{"key":"B5","doi-asserted-by":"publisher","first-page":"1","DOI":"10.1155\/2014\/590409","article-title":"Interactions between Neutrophils, Th17 Cells, and Chemokines during the Initiation of Experimental Model of Multiple Sclerosis","volume":"2014","author":"Wojkowska","year":"2014","journal-title":"Mediators Inflammation"},{"key":"B6","doi-asserted-by":"publisher","first-page":"1","DOI":"10.1155\/2014\/285245","article-title":"The Contribution of Immune and Glial Cell Types in Experimental Autoimmune Encephalomyelitis and Multiple Sclerosis","volume":"2014","author":"Duffy","year":"2014","journal-title":"Mult Scler Int"},{"key":"B7","doi-asserted-by":"publisher","DOI":"10.3109\/17482968.2012.665929","article-title":"Inappropriately chelated iron in the cerebrospinal fluid of amyotrophic lateral sclerosis patients","volume":"13","author":"Ignjatovi\u0107","year":"2012","journal-title":"Amyotroph Lateral Scler"},{"key":"B8","doi-asserted-by":"publisher","DOI":"10.1038\/nature08478","article-title":"Effector T cell interactions with meningeal vascular structures in nascent autoimmune CNS lesions","volume":"462","author":"Bartholom\u00e4us","year":"2009","journal-title":"Nature"},{"key":"B9","doi-asserted-by":"publisher","DOI":"10.1191\/135248506ms1304rr","article-title":"The macrophage in MS: Just a scavenger after all? 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