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Proc Natl Acad Sci U S A. 2017 May 9;114(19):4999-5004. doi: 10.1073/pnas.1620774114. Epub 2017 Apr 24.

Gestational bisphenol-A exposure lowers the threshold for autoimmunity in a model of multiple sclerosis.

Author information

1
Hotchkiss Brain Institute and the Department of Clinical Neurosciences, Cumming School of Medicine, University of Calgary, Calgary, AB T2N 4N1, Canada.
2
Department of Biochemistry and Molecular Biology, Cumming School of Medicine, University of Calgary, Calgary, AB T2N 1N4, Canada.
3
Department of Comparative Biology and Experimental Medicine, Faculty of Veterinary Medicine, University of Calgary, Calgary, AB T2N 1N4, Canada.
4
Hotchkiss Brain Institute and the Department of Clinical Neurosciences, Cumming School of Medicine, University of Calgary, Calgary, AB T2N 4N1, Canada; vyong@ucalgary.ca.

Abstract

Environmental and hormonal factors are implicated in dysimmunity in multiple sclerosis. We investigated whether bisphenol-A, a prominent contaminant with endocrine-disrupting capabilities, altered susceptibility in an inflammatory model of multiple sclerosis. We found that gestational, but not adult, exposure to bisphenol-A increased the development of experimental autoimmune encephalomyelitis in adulthood in male, but not female, mice when a suboptimal disease-inducing immunization was used. Gestational bisphenol-A in male mice primed macrophages in adulthood and raised granulocyte-colony stimulating factor and neutrophil counts/activity postsuboptimal immunization. Neutralizing granulocyte-colony stimulating factor blocked susceptibility to disease in bisphenol-A mice. Early life exposure to bisphenol-A may represent an environmental consideration in multiple sclerosis.

KEYWORDS:

bisphenol A; experimental autoimmune encephalomyelitis; gestational exposure; innate immunity; multiple sclerosis

PMID:
28439012
PMCID:
PMC5441731
DOI:
10.1073/pnas.1620774114
[Indexed for MEDLINE]
Free PMC Article

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