TitleThe vitamin D-antimicrobial peptide pathway and its role in protection against infection.
Publication TypeJournal Article
Year of Publication2009
AuthorsGombart AF
JournalFuture Microbiol
Date Published2009 Nov
KeywordsAnimals, Antimicrobial Cationic Peptides, Bacterial Infections, Cathelicidins, Gene Expression Regulation, Humans, Immunity, Innate, Metabolic Networks and Pathways, Receptors, Calcitriol, Vitamin D, Vitamin D Deficiency, Vitamins

Vitamin D deficiency has been correlated with increased rates of infection. Since the early 19th century, both environmental (i.e., sunlight) and dietary sources (cod liver) of vitamin D have been identified as treatments for TB. The recent discovery that vitamin D induces antimicrobial peptide gene expression explains, in part, the 'antibiotic' effect of vitamin D and has greatly renewed interest in the ability of vitamin D to improve immune function. Subsequent work indicates that this regulation is biologically important for the response of the innate immune system to wounds and infection and that deficiency may lead to suboptimal responses toward bacterial and viral infections. The regulation of the cathelicidin antimicrobial peptide gene is a human/primate-specific adaptation and is not conserved in other mammals. The capacity of the vitamin D receptor to act as a high-affinity receptor for vitamin D and a low-affinity receptor for secondary bile acids and potentially other novel nutritional compounds suggests that the evolutionary selection to place the cathelicidin gene under control of the vitamin D receptor allows for its regulation under both endocrine and xenobiotic response systems. Future studies in both humans and humanized mouse models will elucidate the importance of this regulation and lead to the development of potential therapeutic applications.

Alternate JournalFuture Microbiol
PubMed ID19895218
PubMed Central IDPMC2821804
Grant ListR01 AI065604 / AI / NIAID NIH HHS / United States
R01 AI065604-04 / AI / NIAID NIH HHS / United States
5R01AI065604-04 / AI / NIAID NIH HHS / United States