Prenatal cadmium exposure does not induce greater incidence or earlier onset of autoimmunity in the offspring.

We previously demonstrated that exposure of adult mice to environmental levels of cadmium (Cd) alters immune cell development and function with increases in anti-streptococcal antibody levels, as well as decreases in splenic natural regulatory T cells (nTreg) in the adult female offspring. Based on...

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Autores principales:	Jamie L McCall, Harry C Blair, Kathryn E Blethen, Casey Hall, Meenal Elliott, John B Barnett
Formato:	article
Lenguaje:	EN
Publicado:	Public Library of Science (PLoS) 2021
Materias:	Medicine R Science Q
Acceso en línea:	https://doaj.org/article/04f7e17cd38d4040a4abaf4e9578d319
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spelling	oai:doaj.org-article:04f7e17cd38d4040a4abaf4e9578d3192021-12-02T20:08:31ZPrenatal cadmium exposure does not induce greater incidence or earlier onset of autoimmunity in the offspring.1932-620310.1371/journal.pone.0249442https://doaj.org/article/04f7e17cd38d4040a4abaf4e9578d3192021-01-01T00:00:00Zhttps://doi.org/10.1371/journal.pone.0249442https://doaj.org/toc/1932-6203We previously demonstrated that exposure of adult mice to environmental levels of cadmium (Cd) alters immune cell development and function with increases in anti-streptococcal antibody levels, as well as decreases in splenic natural regulatory T cells (nTreg) in the adult female offspring. Based on these data, we hypothesized that prenatal Cd exposure could predispose an individual to developing autoimmunity as adults. To test this hypothesis, the effects of prenatal Cd on the development of autoimmune diabetes and arthritis were investigated. Non-obese diabetic (NOD) mice were exposed to Cd in a manner identical to our previous studies, and the onset of diabetes was assessed in the offspring. Our results showed a similar time-to-onset and severity of disease to historical data, and there were no statistical differences between Cd-exposed and control offspring. Numerous other immune parameters were measured and none of these parameters showed biologically-relevant differences between Cd-exposed and control animals. To test whether prenatal Cd-exposure affected development of autoimmune arthritis, we used SKG mice. While the levels of arthritis were similar between Cd-exposed and control offspring of both sexes, the pathology of arthritis determined by micro-computed tomography (μCT) between Cd-exposed and control animals, showed some statistically different values, especially in the female offspring. However, the differences were small and thus, the biological significance of these changes is open to speculation. Overall, based on the results from two autoimmune models, we conclude that prenatal exposure to Cd did not lead to a measurable propensity to develop autoimmune disease later in life.Jamie L McCallHarry C BlairKathryn E BlethenCasey HallMeenal ElliottJohn B BarnettPublic Library of Science (PLoS)articleMedicineRScienceQENPLoS ONE, Vol 16, Iss 9, p e0249442 (2021)
institution	DOAJ
collection	DOAJ
language	EN
topic	Medicine R Science Q
spellingShingle	Medicine R Science Q Jamie L McCall Harry C Blair Kathryn E Blethen Casey Hall Meenal Elliott John B Barnett Prenatal cadmium exposure does not induce greater incidence or earlier onset of autoimmunity in the offspring.
description	We previously demonstrated that exposure of adult mice to environmental levels of cadmium (Cd) alters immune cell development and function with increases in anti-streptococcal antibody levels, as well as decreases in splenic natural regulatory T cells (nTreg) in the adult female offspring. Based on these data, we hypothesized that prenatal Cd exposure could predispose an individual to developing autoimmunity as adults. To test this hypothesis, the effects of prenatal Cd on the development of autoimmune diabetes and arthritis were investigated. Non-obese diabetic (NOD) mice were exposed to Cd in a manner identical to our previous studies, and the onset of diabetes was assessed in the offspring. Our results showed a similar time-to-onset and severity of disease to historical data, and there were no statistical differences between Cd-exposed and control offspring. Numerous other immune parameters were measured and none of these parameters showed biologically-relevant differences between Cd-exposed and control animals. To test whether prenatal Cd-exposure affected development of autoimmune arthritis, we used SKG mice. While the levels of arthritis were similar between Cd-exposed and control offspring of both sexes, the pathology of arthritis determined by micro-computed tomography (μCT) between Cd-exposed and control animals, showed some statistically different values, especially in the female offspring. However, the differences were small and thus, the biological significance of these changes is open to speculation. Overall, based on the results from two autoimmune models, we conclude that prenatal exposure to Cd did not lead to a measurable propensity to develop autoimmune disease later in life.
format	article
author	Jamie L McCall Harry C Blair Kathryn E Blethen Casey Hall Meenal Elliott John B Barnett
author_facet	Jamie L McCall Harry C Blair Kathryn E Blethen Casey Hall Meenal Elliott John B Barnett
author_sort	Jamie L McCall
title	Prenatal cadmium exposure does not induce greater incidence or earlier onset of autoimmunity in the offspring.
title_short	Prenatal cadmium exposure does not induce greater incidence or earlier onset of autoimmunity in the offspring.
title_full	Prenatal cadmium exposure does not induce greater incidence or earlier onset of autoimmunity in the offspring.
title_fullStr	Prenatal cadmium exposure does not induce greater incidence or earlier onset of autoimmunity in the offspring.
title_full_unstemmed	Prenatal cadmium exposure does not induce greater incidence or earlier onset of autoimmunity in the offspring.
title_sort	prenatal cadmium exposure does not induce greater incidence or earlier onset of autoimmunity in the offspring.
publisher	Public Library of Science (PLoS)
publishDate	2021
url	https://doaj.org/article/04f7e17cd38d4040a4abaf4e9578d319
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Prenatal cadmium exposure does not induce greater incidence or earlier onset of autoimmunity in the offspring.

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