Format

Send to

Choose Destination
See comment in PubMed Commons below
Arch Biochem Biophys. 2007 Apr 15;460(2):306-13. Epub 2007 Jan 2.

Vitamin D receptor expression by the lung micro-environment is required for maximal induction of lung inflammation.

Author information

1
Department of Veterinary and Biomedical Science, The Center for Molecular Immunology and Infectious Disease, The Pennsylvania State University, University Park, PA 16802, USA.

Abstract

Mice lacking the vitamin D receptor (VDR) are resistant to airway inflammation. Pathogenic immune cells capable of transferring experimental airway inflammation to wildtype (WT) mice are present and primed in the VDR KO mice. Furthermore, the VDR KO immune cells homed to the WT lung in sufficient numbers to induce symptoms of asthma. Conversely, WT splenocytes, Th2 cells and hematopoetic cells induced some symptoms of experimental asthma when transferred to VDR KO mice, but the severity was less than that seen in the WT controls. Interestingly, experimentally induced vitamin D deficiency failed to mirror the VDR KO phenotype suggesting there might be a difference between absence of the ligand and VDR deficiency. Lipopolysaccharide (LPS) induced inflammation in the lungs of VDR KO mice was also less than in WT mice. Together the data suggest that vitamin D and the VDR are important regulators of inflammation in the lung and that in the absence of the VDR the lung environment, independent of immune cells, is less responsive to environmental challenges.

PMID:
17224129
PMCID:
PMC1933487
DOI:
10.1016/j.abb.2006.12.011
[Indexed for MEDLINE]
Free PMC Article
PubMed Commons home

PubMed Commons

0 comments
How to join PubMed Commons

    Supplemental Content

    Full text links

    Icon for Elsevier Science Icon for PubMed Central
    Loading ...
    Support Center