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Prenatal vitamin D deficiency induces an early and more severe experimental autoimmune encephalomyelitis in the second generation.

Fernandes de Abreu DA, Landel V, Barnett AG, McGrath J, Eyles D, Feron F - Int J Mol Sci (2012)

Bottom Line: We then wondered whether a similar response was observed in the subsequent generation.A trend for a reduced number of births in the Fall for the parents of MS patients was observed but statistical significance was not reached.Further well powered studies are warranted to validate the latter finding.

View Article: PubMed Central - PubMed

Affiliation: Neurobiology of Cell Interactions and Neurophysiopathology, Centre National de la Recherche Scientifique, UMR 7259, Aix Marseille Université, Marseille 13015, France; E-Mails: diana.fernandes_de_abreu@kcl.ac.uk (D.A.F.A.); verena.landel@univ-amu.fr (V.L.).

ABSTRACT
In a previous study, we demonstrated that mouse adult F(1) offspring, exposed to a vitamin D deficiency during pregnancy, developed a less severe and delayed Experimental Autoimmune Encephalomyelitis (EAE), when compared with control offspring. We then wondered whether a similar response was observed in the subsequent generation. To answer this question, we assessed F(2) females whose F(1) parents (males or females) were vitamin D-deprived when developing in the uterus of F(0) females. Unexpectedly, we observed that the vitamin D deficiency affecting the F(0) pregnant mice induced a precocious and more severe EAE in the F(2) generation. This paradoxical finding led us to assess its implications for the epidemiology of Multiple Sclerosis (MS) in humans. Using the REFGENSEP database for MS trios (the patient and his/her parents), we collected the parents' dates of birth and assessed a potential season of birth effect that could potentially be indicative of the vitamin D status of the pregnant grandmothers. A trend for a reduced number of births in the Fall for the parents of MS patients was observed but statistical significance was not reached. Further well powered studies are warranted to validate the latter finding.

No MeSH data available.


Related in: MedlinePlus

Clinical course of MOG35-55-induced EAE in F2 mice. F2 female mice born to either a DVD-deficient F1 Mother or a DVD-deficient F1 Father display an early and more severe EAE when compared with control mice.
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f2-ijms-13-10911: Clinical course of MOG35-55-induced EAE in F2 mice. F2 female mice born to either a DVD-deficient F1 Mother or a DVD-deficient F1 Father display an early and more severe EAE when compared with control mice.

Mentions: The three tested groups developed MOG35-55-induced EAE (Figure 2). However, DVD-deficiency in the F0 generation significantly altered the EAE course in the F2 generation. Female F2 offspring from both DVD-deficient maternal and paternal sources developed a measurable EAE (i.e., level 1) with a significantly earlier onset (onset day 13.7 ± 0.4 and 13.4 ± 0.5, respectively) when compared to controls (onset day 16.3 ± 0.6, F = 8.6, p = 0.0011). Moreover, both DVD groups displayed an increased peak in clinical score (3.1 ± 0.3 and 3.4 ± 0.5, respectively) when compared to controls (1.6 ± 0.4, F = 5.95, p = 0.0066). At Day0 of immunization, the mean weight of the three tested groups was similar (DVD Mother: 19.2 ± 0.5; DVD Father: 20.7 ± 0.4 g; controls: 21.2 ± 0.9).


Prenatal vitamin D deficiency induces an early and more severe experimental autoimmune encephalomyelitis in the second generation.

Fernandes de Abreu DA, Landel V, Barnett AG, McGrath J, Eyles D, Feron F - Int J Mol Sci (2012)

Clinical course of MOG35-55-induced EAE in F2 mice. F2 female mice born to either a DVD-deficient F1 Mother or a DVD-deficient F1 Father display an early and more severe EAE when compared with control mice.
© Copyright Policy - open-access
Related In: Results  -  Collection

License 1 - License 2
Show All Figures
getmorefigures.php?uid=PMC3472720&req=5

f2-ijms-13-10911: Clinical course of MOG35-55-induced EAE in F2 mice. F2 female mice born to either a DVD-deficient F1 Mother or a DVD-deficient F1 Father display an early and more severe EAE when compared with control mice.
Mentions: The three tested groups developed MOG35-55-induced EAE (Figure 2). However, DVD-deficiency in the F0 generation significantly altered the EAE course in the F2 generation. Female F2 offspring from both DVD-deficient maternal and paternal sources developed a measurable EAE (i.e., level 1) with a significantly earlier onset (onset day 13.7 ± 0.4 and 13.4 ± 0.5, respectively) when compared to controls (onset day 16.3 ± 0.6, F = 8.6, p = 0.0011). Moreover, both DVD groups displayed an increased peak in clinical score (3.1 ± 0.3 and 3.4 ± 0.5, respectively) when compared to controls (1.6 ± 0.4, F = 5.95, p = 0.0066). At Day0 of immunization, the mean weight of the three tested groups was similar (DVD Mother: 19.2 ± 0.5; DVD Father: 20.7 ± 0.4 g; controls: 21.2 ± 0.9).

Bottom Line: We then wondered whether a similar response was observed in the subsequent generation.A trend for a reduced number of births in the Fall for the parents of MS patients was observed but statistical significance was not reached.Further well powered studies are warranted to validate the latter finding.

View Article: PubMed Central - PubMed

Affiliation: Neurobiology of Cell Interactions and Neurophysiopathology, Centre National de la Recherche Scientifique, UMR 7259, Aix Marseille Université, Marseille 13015, France; E-Mails: diana.fernandes_de_abreu@kcl.ac.uk (D.A.F.A.); verena.landel@univ-amu.fr (V.L.).

ABSTRACT
In a previous study, we demonstrated that mouse adult F(1) offspring, exposed to a vitamin D deficiency during pregnancy, developed a less severe and delayed Experimental Autoimmune Encephalomyelitis (EAE), when compared with control offspring. We then wondered whether a similar response was observed in the subsequent generation. To answer this question, we assessed F(2) females whose F(1) parents (males or females) were vitamin D-deprived when developing in the uterus of F(0) females. Unexpectedly, we observed that the vitamin D deficiency affecting the F(0) pregnant mice induced a precocious and more severe EAE in the F(2) generation. This paradoxical finding led us to assess its implications for the epidemiology of Multiple Sclerosis (MS) in humans. Using the REFGENSEP database for MS trios (the patient and his/her parents), we collected the parents' dates of birth and assessed a potential season of birth effect that could potentially be indicative of the vitamin D status of the pregnant grandmothers. A trend for a reduced number of births in the Fall for the parents of MS patients was observed but statistical significance was not reached. Further well powered studies are warranted to validate the latter finding.

No MeSH data available.


Related in: MedlinePlus