Vitamin D receptor expression by the lung micro-environment is required for maximal induction of lung inflammation. Journal   Archives of biochemistry and biophysics. Citation   Arch Biochem Biophys. 460(2):306-13 Publication date   2007 Apr 15 Authors   Wittke A Chang A Froicu M Harandi OF Weaver V August A Paulson RF Cantorna MT Investigators   Avery August Margherita Cantorna Robert Paulson Grant agencies   National Institute of Neurological Disorders and Stroke Grants   NINDS R01 NS038888-04 MeSH headings   Asthma Hematopoietic Stem Cells Immunity, Natural Receptors, Calcitriol Th2 Cells Vitamin D MeSH qualifiers   immunology 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.