PDCB does not promote CNS autoimmunity in the context of genetic susceptibility but worsens its outcome

• Published in: Journal of neuroimmunology 2018-10, Vol.323, p.53-55
• Main Authors: Dubey, Divyanshu, Hussain, Rehana Z., Miller-Little, William A., Salter, Amber, Doelger, Richard, Stüve, Olaf
• Format: Article
• Language: English
• ISSN: 0165-5728; 1872-8421
• DOI: 10.1016/j.jneuroim.2018.07.012

Para-dichlorobenzene (PDCB) is an aromatic hydrocarbon contained in mothballs that is potentially neurotoxic. A potential pathogenic role of PDCB in MS pathogenesis has been suggested. To determine the ability of chronic PDCB ingestion to induce CNS autoimmunity in a genetically susceptible mammalian species, naive myelin oligodendrocyte glycoprotein peptide (MOGp)35–55 T cell receptor (TCR) transgenic mice (2D2) on the C57Bl/6 background were orally gavaged once daily with corn oil control, 125 mg/kg PDCB, or 250 mg/kg PDCB for 45 days. The incidence of spontaneous EAE is increased in this mouse strain. Both PDCB treatment groups showed the same spontaneous incidence of EAE, an earlier disease onset, and a slight decrease in survival for 125 mg/kg PDCB mice compared to control mice. We were unable to detect any PDCB, or its metabolites 2,5-dichlorophenol, 2,5-dicholormethylsulfide, and 2,5-dichloromethylsulfone in the brain and spinal cord of control mice. In contrast, PDCB was readily detectable in both compartments in mice who received PDCB via oral gavage, with concentrations being significantly higher in the brain (p