TY - JOUR
T1 - Vitamin D supplementation protects against bone loss following inhalant organic dust and lipopolysaccharide exposures in mice
AU - Dusad, Anand
AU - Thiele, Geoffrey Milton
AU - Klassen, Lynell Warren
AU - Wang, Dong
AU - Duryee, Michael J.
AU - Mikuls, Ted R
AU - Staab, Elizabeth B.
AU - Wyatt, Todd A
AU - West, William W.
AU - Reynolds, Stephen J.
AU - Romberger, Debra
AU - Poole, Jill A
N1 - Funding Information:
This material is the result of work supported with resources and the use of facilities at the VA Nebraska-Western Iowa Health Care System, Omaha, NE. This study was supported by Grants from the American College of Rheumatology/Rheumatology Research Foundation, Department of Internal Medicine, University of Nebraska Medical Center, Nebraska Arthritis Outcomes Research Center, National Institute of Arthritis and Musculoskeletal Diseases, and National Institute of Environmental Health Sciences. This work was also supported in part by the Central States Center for Agricultural Safety and Health (CS-CASH).
Publisher Copyright:
© 2015, Springer Science+Business Media New York.
PY - 2015/5/1
Y1 - 2015/5/1
N2 - Systemic bone loss is associated with airway inflammatory diseases; yet, strategies to halt disease progression from inhalant exposures are not clear. Vitamin D might be a potentially protective approach against noxious respirable environmental exposures. We sought to determine whether vitamin D supplementation represents a viable lung- and bone-protective strategy following repetitive inhalant treatments with organic dust extract (ODE) or lipopolysaccharide (LPS) in mice. C57BL/5 mice were maintained on diets with low (1 IU/D/g) or high (10 IU/D/g) vitamin D for 5 weeks and treated with ODE from swine confinement facilities, LPS, or saline daily for 3 weeks per established intranasal inhalation protocol. Lungs, hind limbs, and sera were harvested for experimental outcomes. Serum 25-hydroxyvitamin D levels were tenfold different between low and high vitamin D treatment groups with no differences between inhalant agents and saline treatments. Serum calcium levels were not affected. There was no difference in the magnitude of ODE- or LPS-induced inflammatory cell influx or lung histopathology between high and low vitamin D treatment groups. However, high vitamin D treatment reversed the loss of bone mineral density, bone volume, and bone micro-architecture deterioration induced by ODE or LPS as determined by micro-CT analysis. Bone-resorbing osteoclasts were also reduced by high vitamin D treatment. In the low vitamin D treatment groups, ODE induced the greatest degree of airway inflammatory consequences, and LPS induced the greatest degree of bone loss. Collectively, high-concentration vitamin D was protective against systemic bone loss, but not airway inflammation, resulting from ODE- or LPS-induced airway injury.
AB - Systemic bone loss is associated with airway inflammatory diseases; yet, strategies to halt disease progression from inhalant exposures are not clear. Vitamin D might be a potentially protective approach against noxious respirable environmental exposures. We sought to determine whether vitamin D supplementation represents a viable lung- and bone-protective strategy following repetitive inhalant treatments with organic dust extract (ODE) or lipopolysaccharide (LPS) in mice. C57BL/5 mice were maintained on diets with low (1 IU/D/g) or high (10 IU/D/g) vitamin D for 5 weeks and treated with ODE from swine confinement facilities, LPS, or saline daily for 3 weeks per established intranasal inhalation protocol. Lungs, hind limbs, and sera were harvested for experimental outcomes. Serum 25-hydroxyvitamin D levels were tenfold different between low and high vitamin D treatment groups with no differences between inhalant agents and saline treatments. Serum calcium levels were not affected. There was no difference in the magnitude of ODE- or LPS-induced inflammatory cell influx or lung histopathology between high and low vitamin D treatment groups. However, high vitamin D treatment reversed the loss of bone mineral density, bone volume, and bone micro-architecture deterioration induced by ODE or LPS as determined by micro-CT analysis. Bone-resorbing osteoclasts were also reduced by high vitamin D treatment. In the low vitamin D treatment groups, ODE induced the greatest degree of airway inflammatory consequences, and LPS induced the greatest degree of bone loss. Collectively, high-concentration vitamin D was protective against systemic bone loss, but not airway inflammation, resulting from ODE- or LPS-induced airway injury.
KW - Bone interactors-other systems biology
KW - Osteoporosis disease disorder
KW - Preclinical animal models
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U2 - 10.1007/s12026-015-8634-4
DO - 10.1007/s12026-015-8634-4
M3 - Article
C2 - 25759026
AN - SCOPUS:84939947335
SN - 0257-277X
VL - 62
SP - 46
EP - 59
JO - Immunologic Research
JF - Immunologic Research
IS - 1
ER -