Lipopolysaccharide-induced lung injury is independent of serum vitamin D concentration.

Vitamin D deficiency is increasing in incidence around the world. Vitamin D, a fat-soluble vitamin, has documented effects on the innate and adaptive immune system, including macrophage and T regulatory (Treg) cell function. Since Treg cells are important in acute lung injury resolution, we hypothes...

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Autores principales:	Lindy S Klaff, Sean E Gill, Brent E Wisse, Kristen Mittelsteadt, Gustavo Matute-Bello, Peter Chen, William A Altemeier
Formato:	article
Lenguaje:	EN
Publicado:	Public Library of Science (PLoS) 2012
Materias:	Medicine R Science Q
Acceso en línea:	https://doaj.org/article/f8f37567d36c4716887791ca7e85abdd
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spelling	oai:doaj.org-article:f8f37567d36c4716887791ca7e85abdd2021-11-18T08:08:19ZLipopolysaccharide-induced lung injury is independent of serum vitamin D concentration.1932-620310.1371/journal.pone.0049076https://doaj.org/article/f8f37567d36c4716887791ca7e85abdd2012-01-01T00:00:00Zhttps://www.ncbi.nlm.nih.gov/pmc/articles/pmid/23185294/?tool=EBIhttps://doaj.org/toc/1932-6203Vitamin D deficiency is increasing in incidence around the world. Vitamin D, a fat-soluble vitamin, has documented effects on the innate and adaptive immune system, including macrophage and T regulatory (Treg) cell function. Since Treg cells are important in acute lung injury resolution, we hypothesized that vitamin D deficiency increases the severity of injury and delays injury resolution in lipopolysaccharide (LPS) induced acute lung injury. Vitamin D deficient mice were generated, using C57BL/6 mice, through diet modification and limited exposure to ultraviolet light. At 8 weeks of age, vitamin D deficient and sufficient mice received 2.5 g/kg of LPS or saline intratracheal. At 1 day, 3 days and 10 days, mice were anesthetized and lung elastance measured. Mice were euthanized and bronchoalveolar lavage fluid, lungs and serum were collected. Ex vivo neutrophil chemotaxis was evaluated, using neutrophils from vitamin D sufficient and deficient mice exposed to the chemoattractants, KC/CXCL1 and C5a, and to bronchoalveolar lavage fluid from LPS-exposed mice. We found no difference in the degree of lung injury. Leukocytes were mildly decreased in the bronchoalveolar fluid of vitamin D deficient mice at 1 day. Ex-vivo, neutrophils from vitamin D deficient mice showed impaired chemotaxis to KC but not to C5a. Vitamin D deficiency modestly impairs neutrophil chemotaxis; however, it does not affect lung injury or its resolution in an LPS model of acute lung injury.Lindy S KlaffSean E GillBrent E WisseKristen MittelsteadtGustavo Matute-BelloPeter ChenWilliam A AltemeierPublic Library of Science (PLoS)articleMedicineRScienceQENPLoS ONE, Vol 7, Iss 11, p e49076 (2012)
institution	DOAJ
collection	DOAJ
language	EN
topic	Medicine R Science Q
spellingShingle	Medicine R Science Q Lindy S Klaff Sean E Gill Brent E Wisse Kristen Mittelsteadt Gustavo Matute-Bello Peter Chen William A Altemeier Lipopolysaccharide-induced lung injury is independent of serum vitamin D concentration.
description	Vitamin D deficiency is increasing in incidence around the world. Vitamin D, a fat-soluble vitamin, has documented effects on the innate and adaptive immune system, including macrophage and T regulatory (Treg) cell function. Since Treg cells are important in acute lung injury resolution, we hypothesized that vitamin D deficiency increases the severity of injury and delays injury resolution in lipopolysaccharide (LPS) induced acute lung injury. Vitamin D deficient mice were generated, using C57BL/6 mice, through diet modification and limited exposure to ultraviolet light. At 8 weeks of age, vitamin D deficient and sufficient mice received 2.5 g/kg of LPS or saline intratracheal. At 1 day, 3 days and 10 days, mice were anesthetized and lung elastance measured. Mice were euthanized and bronchoalveolar lavage fluid, lungs and serum were collected. Ex vivo neutrophil chemotaxis was evaluated, using neutrophils from vitamin D sufficient and deficient mice exposed to the chemoattractants, KC/CXCL1 and C5a, and to bronchoalveolar lavage fluid from LPS-exposed mice. We found no difference in the degree of lung injury. Leukocytes were mildly decreased in the bronchoalveolar fluid of vitamin D deficient mice at 1 day. Ex-vivo, neutrophils from vitamin D deficient mice showed impaired chemotaxis to KC but not to C5a. Vitamin D deficiency modestly impairs neutrophil chemotaxis; however, it does not affect lung injury or its resolution in an LPS model of acute lung injury.
format	article
author	Lindy S Klaff Sean E Gill Brent E Wisse Kristen Mittelsteadt Gustavo Matute-Bello Peter Chen William A Altemeier
author_facet	Lindy S Klaff Sean E Gill Brent E Wisse Kristen Mittelsteadt Gustavo Matute-Bello Peter Chen William A Altemeier
author_sort	Lindy S Klaff
title	Lipopolysaccharide-induced lung injury is independent of serum vitamin D concentration.
title_short	Lipopolysaccharide-induced lung injury is independent of serum vitamin D concentration.
title_full	Lipopolysaccharide-induced lung injury is independent of serum vitamin D concentration.
title_fullStr	Lipopolysaccharide-induced lung injury is independent of serum vitamin D concentration.
title_full_unstemmed	Lipopolysaccharide-induced lung injury is independent of serum vitamin D concentration.
title_sort	lipopolysaccharide-induced lung injury is independent of serum vitamin d concentration.
publisher	Public Library of Science (PLoS)
publishDate	2012
url	https://doaj.org/article/f8f37567d36c4716887791ca7e85abdd
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Lipopolysaccharide-induced lung injury is independent of serum vitamin D concentration.

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