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Dietary supplementation with white button mushroom enhances natural killer cell activity in C57BL/6 mice. Wu D, Pae M, Ren Z, Guo Z, Smith D, Meydani SN. J Nutr. 2007 Jun;137(6):1472-7. PMID: 17513409

White button mushroom enhances maturation of bone marrow-derived dendritic cells and their antigen presenting function in mice.\nRen Z, Guo Z, Meydani SN, Wu D.\nJ Nutr. 2008 Mar;138(3):544-50.\nPMID: 18287364

P.T. Liu, S. Stenger, H. Li, L. Wenzel, B.H. Tan, S.R. Krutzik, M.T. Ochoa, J. Schauber, K. Wu, C. Meinken, et al.\nVitamin D3-Triggered Antimicrobial Response--Another Pleiotropic Effect beyond Mineral and Bone Metabolism: Toll-Like Receptor Triggering of a Vitamin D-Mediated Human Antimicrobial Response. Science 311: 1770-1773, 2006\nJ. Am. Soc. Nephrol., November 1, 2006; 17(11): 2949 - 2953.

'Vitamin D Induces Innate Antibacterial Responses in Human Trophoblasts via an Intracrine Pathway.\nLiu N, Kaplan AT, Low J, Nguyen L, Liu GY, Equils O, Hewison M.\nBiol Reprod. 2009 Mar;80(3):398-406. Epub 2008 Nov 12.\nPMID: 19005165DOI: 10.1095/biolreprod.108.073577

Back to the future: a new look at 'old' vitamin D. Chun RF, Adams JS, Hewison M. J Endocrinol. 2008 Aug;198(2):261-9. Epub 2008 May 21. PMID: 18495944 DOI: 10.1677/JOE-08-0170

Cutting edge: vitamin D-mediated human antimicrobial activity against Mycobacterium tuberculosis is dependent on the induction of cathelicidin.\nLiu PT, Stenger S, Tang DH, Modlin RL.\nJ Immunol. 2007 Aug 15;179(4):2060-3.\nPMID: 1767546

Vitamin D in defense of the human immune response.\nAdams JS, Liu PT, Chun R, Modlin RL, Hewison M.\nAnn N Y Acad Sci. 2007 Nov;1117:94-105. Epub 2007 Jul 26. Review.\nPMID: 17656563\nDOI: 10.1196/annals.1402.03

Vitamin D supplementation to prevent infections: a sub-study of a randomised placebo-controlled trial in older people (RECORD trial, ISRCTN 51647438).\nAvenell A, Cook JA, Maclennan GS, Macpherson GC.\nAge Ageing. 2007 Sep;36(5):574-7. Epub 2007 Aug 15. No abstract available.\nPMID: 17702768 \ndoi:10.1093/ageing/afm091

Vitamin D signaling, infectious diseases, and regulation of innate immunity. White JH. Infect Immun. 2008 Sep;76(9):3837-43. Epub 2008 May 27. Review. PMID: 18505808 doi:10.1128/IAI.00353-08

Human cathelicidin antimicrobial peptide (CAMP) gene is a direct target of the vitamin D receptor and is strongly up-regulated in myeloid cells by 1,25-dihydroxyvitamin D3.\nGombart AF, Borregaard N, Koeffler HP.\nFASEB J. 2005 Jul;19(9):1067-77.\nPMID: 15985530

On the epidemiology of influenza. Cannell JJ, Zasloff M, Garland CF, Scragg R, Giovannucci E. Virol J. 2008 Feb 25;5:29. Review. PMID: 18298852 doi:10.1186/1743-422X-5-29

Association Between Serum 25-Hydroxyvitamin D Level and Upper Respiratory Tract Infection. \nAdit A. Ginde, MD, MPH; Jonathan M. Mansbach, MD; Carlos A. Camargo Jr, MD, DrPH . \nArch Intern Med. 2009;169(4):384-390\n

Vitamin D may suppress infections which lead to development of Multiple Sclerosis Steven R Brenner, None (16 August 2007) J Neurol Neurosurg Psychiatry 2008 I read the article with reference to the inverse relationship between multiple sclerosis clinical activity and deficiency of vitamin D by Soilu-Hannienen (1) with interest, and was considering what mechanism could be in play to cause such a relationship. 25-hydroxylated metabolites of vitamin D act as intracellular regulators of the synthesis and action of defensin (2) molecules against bacterial antigens, defensin being an endogenously synthesized antimicrobial substance (2). Human cathelicidin antimicrobial peptide gene is a target of vitamin D receptor and is strongly up-regulated by 1,25-dihydroxyvitamin D3, indicating vitamin D receptor and the 1,25-dihydroxyvitaminD3 regulate primate innate immunity (3)

Conclusion The data point to a critical role for the VDR and 1,25(OH)2D3 in control of innate immunity and the response of the colon to chemical injury. Vitamin D and the vitamin D receptor are critical for control of the innate immune response to colonic injury. Froicu M, Cantorna MT. BMC Immunol. 2007 Mar 30;8:5. PMID: 17397543 doi:10.1186/1471-2172-8-5

Conclusion We demonstrated that the VDRE in the CAMP gene originated from the exaptation of an AluSx SINE in the lineage leading to humans, apes, OWMs and NWMs and remained under purifying selection for the last 55-60 million years. We present convincing evidence of an evolutionarily fixed, Alu-mediated divergence in steroid hormone nuclear receptor gene regulation between humans/primates and other mammals. Evolutionary selection to place the primate CAMP gene under regulation of the vitamin D pathway potentiates the innate immune response and may counter the anti-inflammatory properties of vitamin D. Exaptation of an ancient Alu short interspersed element provides a highly conserved vitamin D-mediated innate immune response in humans and primates. Gombart AF, Saito T, Koeffler HP. BMC Genomics. 2009 Jul 16;10:321. PMID: 19607716 doi:10.1186/1471-2164-10-321

A new study has concluded that one key part of the immune system, the ability of vitamin D to regulate anti-bactericidal proteins, is so important that is has been conserved through almost 60 million years of evolution and is shared only by primates, including humans - but no other known animal species.

Native and aspirin-triggered lipoxins control innate immunity by inducing proteasomal degradation of TRAF6. Machado FS, Esper L, Dias A, Madan R, Gu Y, Hildeman D, Serhan CN, Karp CL, Aliberti J. J Exp Med. 2008 May 12;205(5):1077-86. Epub 2008 Apr 14. PMID: 18411340 doi:10.1084/jem.20072416

The vitamin D-antimicrobial peptide pathway and its role in protection against infection. Gombart AF. Future Microbiol. 2009 Nov;4:1151-65. PMID: 19895218 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

"Cathelicidin antimicrobial peptide is a family of polypeptides found in lysosomes in polymorphonuclear leukocytes (PMNs).[1] Members of the cathelicidin family of antimicrobial polypeptides are characterized by a highly conserved region (cathelin domain) and a highly variable cathelicidin peptide domain. Cathelicidin peptides have been isolated from many different species of mammals. Cathelicidins were originally found in neutrophils but have since been found in many other cells including epithelial cells and macrophages activated by bacteria, viruses, fungi, or the hormone 1,25-D"