Journal
MEDIATORS OF INFLAMMATION
Volume 2011, Issue -, Pages -Publisher
HINDAWI LTD
DOI: 10.1155/2011/598345
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Funding
- National Institutes of Health [HD058019, ES005022]
- Foundation of the University of Medicine and Dentistry of New Jersey
- EUNICE KENNEDY SHRIVER NATIONAL INSTITUTE OF CHILD HEALTH &HUMAN DEVELOPMENT [R21HD058019] Funding Source: NIH RePORTER
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Neutrophil activity is prolonged in newborns, suggesting decreased exposure and/or responses to immunosuppressive modulators, such as 1,25-hydroxyvitamin D-3 (1,25-vit D-3). We hypothesized that 1,25-vit D-3 suppresses neutrophil activation and that this response is impaired in newborns. Consistent with this, 1,25-vit D-3 decreased LPS-induced expression of macrophage inflammatory protein-1 beta and VEGF in adult, but not neonatal, neutrophils. Expression of vitamin D receptor (VDR) and 25-hydroxyvitamin D-3-1 alpha-hydroxylase was reduced in neonatal, relative to adult neutrophils. Moreover, 1,25-vit D-3 induced VDR gene expression in activated adult, but not neonatal, neutrophils. 1,25-vit D-3 also suppressed expression of cyclooxygenase-2 and induced expression of 5-lipoxygenase in LPS-exposed adult neutrophils, while neonatal cells were not affected. 1,25-vit D-3 had no effect on respiratory burst in either adult or neonatal cells. Anti-inflammatory activity of vitamin D is impaired in neonatal neutrophils, and this may be due to decreased expression of VDR and 1 alpha-hydroxylase. Insensitivity to 1,25-vit D-3 may contribute to chronic inflammation in neonates.
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