PDCB does not promote CNS autoimmunity in the context of genetic susceptibility but worsens its outcome.
J Neuroimmunol
; 323: 53-55, 2018 10 15.
Article
en En
| MEDLINE
| ID: mdl-30196834
ABSTRACT
BACKGROUND:
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.METHODS:
To determine the ability of chronic PDCB ingestion to induce CNS autoimmunity in a genetically susceptible mammalian species, naive myelin oligodendrocyte glycoprotein peptide (MOGp)35-55â¯T cell receptor (TCR) transgenic mice (2D2) on the C57Bl/6 background were orally gavaged once daily with corn oil control, 125â¯mg/kg PDCB, or 250â¯mg/kg PDCB for 45â¯days. The incidence of spontaneous EAE is increased in this mouse strain.RESULTS:
Both PDCB treatment groups showed the same spontaneous incidence of EAE, an earlier disease onset, and a slight decrease in survival for 125â¯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 (pâ¯<â¯0.01). Levels of the metabolites 2,5-dichlorophenol and 2,5-dichloromethylsulfone were also significantly higher in brains compared to spinal cords.CONCLUSION:
Our study refutes the hypothesis that PDCB or its metabolites trigger spontaneous T cell-mediated CNS autoimmunity in the setting of genetic susceptibility. A slight increase in mortality with PDCB exposure may be due systemic toxicity of hydrocarbons.
Texto completo:
1
Colección:
01-internacional
Base de datos:
MEDLINE
Asunto principal:
Médula Espinal
/
Encéfalo
/
Autoinmunidad
/
Clorobencenos
/
Predisposición Genética a la Enfermedad
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Encefalomielitis Autoinmune Experimental
Límite:
Animals
Idioma:
En
Revista:
J Neuroimmunol
Año:
2018
Tipo del documento:
Article
País de afiliación:
Estados Unidos