Abstract
There is now strong evidence linking vitamin D, the steroid hormone of sunlight, and
Multiple Sclerosis (MS). Two of the most intriguing findings are the season of birth
and childhood sun exposure effects. They both suggest that a vitamin D deficiency
during these critical imprinting periods is a risk factor for MS. After having confirmed
that people born in November are at lower risk of developing MS, we devised a mouse
model of prenatal vitamin D deficiency. We observed that adult offspring born to vitamin
D deficient mothers, when compared to control offspring, developed a striking milder
and delayed experimental autoimmune encephalomyelitis (EAE) and permanently overexpressed
the vitamin D receptor. This unexpected finding led us to conjecture that the newborns,
after having known an in utero vitamin D-deficient environment, were highly sensitive ex utero to cholecalciferol-containing diet and interpreted the postnatal food as a vitamin
D enriched environment. To validate this hypothesis, we devised a mouse model of postnatal
vitamin D supplementation. Interestingly, using the same EAE model, we demonstrated
that a delayed onset and less severe symptoms were displayed by postnatally vitamin
D-supplemented mice. The latter finding is in accordance with previous animal studies
demonstrating that a postnatal vitamin D deficiency induced an earlier onset and an
increased symptom severity of EAE and epidemiological reports describing the importance
of an adequate supply of vitamin D during early life.
Keywords
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Article info
Publication history
Published online: September 19, 2011
Accepted:
August 29,
2011
Received in revised form:
August 23,
2011
Received:
April 29,
2011
Identification
Copyright
© 2011 Elsevier B.V. Published by Elsevier Inc. All rights reserved.