Vitamin D and susceptibility of chronic lung diseases
Isaac K. Sundar and Irfan Rahman
Lung Biology and Disease Program, Department of Environmental Medicine, University of Rochester Medical Center, Rochester, NY, USA

Vitamin D deficiency is linked to accelerated decline in lung function, increased inflammation, and reduced immunity in chronic lung diseases. Epidemiological studies have suggested that vitamin D insufficiency is associated with low lung function in susceptible subjects who are exposed to higher levels of environmental agents (airborne particulates). Recent studies have highlighted the role of vitamin D and vitamin D receptor (VDR) in regulation of several genes that are involved in inflammation, immunity, cellular proliferation, differentiation, and apoptosis. Vitamin D has also been implicated in reversal of steroid resistance and airway remodeling, which are the hallmarks of chronic obstructive pulmonary disease (COPD) and severe asthma.



Role of vitamin D/VDR in environmental agent-mediated deregulation of cellular and molecular functions. Environmental agents such as cigarette smoke, particulate matter (less than 10 μm, PM10), ultrafine particles, inhaled oxidants, ozone, and aldehydes activate vitamin D receptor and affects different downstream cellular and molecular targets as a result of vitamin D-mediated deregulation. The major cellular and molecular function affected due to vitamin D/VDR deregulation includes: calcemic effects, antimicrobial peptide gene activation, tissue remodeling, immune modulation and autoantibody production, muscle function, steroid efficacy, and epigenetic regulation.

Kilde: Vitamin D and susceptibility of chronic lung diseases: role of epigenetics