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

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...

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Published in:	Proceedings of the National Academy of Sciences - PNAS Vol. 114; no. 19; pp. 4999 - 5004
Main Authors:	Rogers, James A., Mishra, Manoj K., Hahn, Jennifer, Greene, Catherine J., Yates, Robin M., Metz, Luanne M., Yong, V. Wee
Format:	Journal Article
Language:	English
Published:	United States National Academy of Sciences 09-05-2017
Subjects:	Animals Autoimmune diseases Autoimmunity Autoimmunity - drug effects Benzhydryl Compounds - toxicity Biological Sciences Bisphenol A Colonies Colony-stimulating factor Contaminants Disease Models, Animal Encephalomyelitis, Autoimmune, Experimental - chemically induced Encephalomyelitis, Autoimmune, Experimental - immunology Encephalomyelitis, Autoimmune, Experimental - pathology Endocrine disruptors Experimental allergic encephalomyelitis Exposure Female Hormones Immunization Inflammation Leukocytes (granulocytic) Macrophages Male Mice Multiple sclerosis Multiple Sclerosis - chemically induced Multiple Sclerosis - immunology Multiple Sclerosis - pathology Neutralizing Phenols - toxicity Pregnancy Prenatal Exposure Delayed Effects - chemically induced Prenatal Exposure Delayed Effects - immunology Prenatal Exposure Delayed Effects - pathology Rodents bisphenol A experimental autoimmune encephalomyelitis innate immunity multiple sclerosis gestational exposure
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Summary:	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.
Bibliography:	ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23 Author contributions: J.A.R., R.M.Y., L.M.M., and V.W.Y. designed research; J.A.R., M.K.M., J.H., and C.J.G. performed research; J.A.R., M.K.M., J.H., C.J.G., R.M.Y., and V.W.Y. analyzed data; and J.A.R., M.K.M., J.H., C.J.G., R.M.Y., L.M.M., and V.W.Y. wrote the paper. Edited by Lawrence Steinman, Stanford University School of Medicine, Stanford, CA, and approved March 16, 2017 (received for review December 17, 2016)
ISSN:	0027-8424 1091-6490
DOI:	10.1073/pnas.1620774114