Acute erythemal ultraviolet radiation causes systemic immunosuppression in the absence of increased 25-hydroxyvitamin D3 levels in male mice.

Vitamin D is synthesised by ultraviolet (UV) irradiation of skin and is hypothesized to be a direct mediator of the immunosuppression that occurs following UV radiation (UVR) exposure. Both UVR and vitamin D drive immune responses towards tolerance by ultimately increasing the suppressive activities...

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Autores principales: Shelley Gorman, Naomi M Scott, Daryl H W Tan, Clare E Weeden, Robert C Tuckey, Jacqueline L Bisley, Michele A Grimbaldeston, Prue H Hart
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Publicado: Public Library of Science (PLoS) 2012
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spelling oai:doaj.org-article:eb8f32f9884f4dccb314bc6c7866870b2021-11-18T08:13:52ZAcute erythemal ultraviolet radiation causes systemic immunosuppression in the absence of increased 25-hydroxyvitamin D3 levels in male mice.1932-620310.1371/journal.pone.0046006https://doaj.org/article/eb8f32f9884f4dccb314bc6c7866870b2012-01-01T00:00:00Zhttps://www.ncbi.nlm.nih.gov/pmc/articles/pmid/23049920/pdf/?tool=EBIhttps://doaj.org/toc/1932-6203Vitamin D is synthesised by ultraviolet (UV) irradiation of skin and is hypothesized to be a direct mediator of the immunosuppression that occurs following UV radiation (UVR) exposure. Both UVR and vitamin D drive immune responses towards tolerance by ultimately increasing the suppressive activities of regulatory T cells. To examine a role for UVR-induced vitamin D, vitamin D(3)-deficient mice were established by dietary vitamin D(3) restriction. In comparison to vitamin D(3)-replete mice, vitamin D(3)-deficient mice had significantly reduced serum levels of 25-hydroxyvitamin D(3) (25(OH)D(3), <20 nmol.L(-1)) and 1,25-dihydroxyvitamin D(3) (1,25(OH)(2)D(3), <20 pmol.L(-1)). Following either acute erythemal UVR, or chronic sub-erythemal UVR (8 exposures over 4 weeks) treatment, serum 25(OH)D(3) levels significantly increased in vitamin D(3)-deficient female but not male mice. To determine if UVR-induced vitamin D was a mediator of UVR-induced systemic immunosuppression, responses were measured in mice that were able (female) or unable (male) to increase systemic levels of 25(OH)D(3) after UVR. Erythemal UVR (≥ 4 kJ/m(2)) suppressed contact hypersensitivity responses (T helper type-1 or -17), aspects of allergic airway disease (T helper type-2) and also the in vivo priming capacity of bone marrow-derived dendritic cells to a similar degree in female and male vitamin D(3)-deficient mice. Thus, in male mice, UVR-induced 25(OH)D(3) is not essential for mediating the immunosuppressive effects of erythemal UVR.Shelley GormanNaomi M ScottDaryl H W TanClare E WeedenRobert C TuckeyJacqueline L BisleyMichele A GrimbaldestonPrue H HartPublic Library of Science (PLoS)articleMedicineRScienceQENPLoS ONE, Vol 7, Iss 9, p e46006 (2012)
institution DOAJ
collection DOAJ
language EN
topic Medicine
R
Science
Q
spellingShingle Medicine
R
Science
Q
Shelley Gorman
Naomi M Scott
Daryl H W Tan
Clare E Weeden
Robert C Tuckey
Jacqueline L Bisley
Michele A Grimbaldeston
Prue H Hart
Acute erythemal ultraviolet radiation causes systemic immunosuppression in the absence of increased 25-hydroxyvitamin D3 levels in male mice.
description Vitamin D is synthesised by ultraviolet (UV) irradiation of skin and is hypothesized to be a direct mediator of the immunosuppression that occurs following UV radiation (UVR) exposure. Both UVR and vitamin D drive immune responses towards tolerance by ultimately increasing the suppressive activities of regulatory T cells. To examine a role for UVR-induced vitamin D, vitamin D(3)-deficient mice were established by dietary vitamin D(3) restriction. In comparison to vitamin D(3)-replete mice, vitamin D(3)-deficient mice had significantly reduced serum levels of 25-hydroxyvitamin D(3) (25(OH)D(3), <20 nmol.L(-1)) and 1,25-dihydroxyvitamin D(3) (1,25(OH)(2)D(3), <20 pmol.L(-1)). Following either acute erythemal UVR, or chronic sub-erythemal UVR (8 exposures over 4 weeks) treatment, serum 25(OH)D(3) levels significantly increased in vitamin D(3)-deficient female but not male mice. To determine if UVR-induced vitamin D was a mediator of UVR-induced systemic immunosuppression, responses were measured in mice that were able (female) or unable (male) to increase systemic levels of 25(OH)D(3) after UVR. Erythemal UVR (≥ 4 kJ/m(2)) suppressed contact hypersensitivity responses (T helper type-1 or -17), aspects of allergic airway disease (T helper type-2) and also the in vivo priming capacity of bone marrow-derived dendritic cells to a similar degree in female and male vitamin D(3)-deficient mice. Thus, in male mice, UVR-induced 25(OH)D(3) is not essential for mediating the immunosuppressive effects of erythemal UVR.
format article
author Shelley Gorman
Naomi M Scott
Daryl H W Tan
Clare E Weeden
Robert C Tuckey
Jacqueline L Bisley
Michele A Grimbaldeston
Prue H Hart
author_facet Shelley Gorman
Naomi M Scott
Daryl H W Tan
Clare E Weeden
Robert C Tuckey
Jacqueline L Bisley
Michele A Grimbaldeston
Prue H Hart
author_sort Shelley Gorman
title Acute erythemal ultraviolet radiation causes systemic immunosuppression in the absence of increased 25-hydroxyvitamin D3 levels in male mice.
title_short Acute erythemal ultraviolet radiation causes systemic immunosuppression in the absence of increased 25-hydroxyvitamin D3 levels in male mice.
title_full Acute erythemal ultraviolet radiation causes systemic immunosuppression in the absence of increased 25-hydroxyvitamin D3 levels in male mice.
title_fullStr Acute erythemal ultraviolet radiation causes systemic immunosuppression in the absence of increased 25-hydroxyvitamin D3 levels in male mice.
title_full_unstemmed Acute erythemal ultraviolet radiation causes systemic immunosuppression in the absence of increased 25-hydroxyvitamin D3 levels in male mice.
title_sort acute erythemal ultraviolet radiation causes systemic immunosuppression in the absence of increased 25-hydroxyvitamin d3 levels in male mice.
publisher Public Library of Science (PLoS)
publishDate 2012
url https://doaj.org/article/eb8f32f9884f4dccb314bc6c7866870b
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