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Vitamin D3 has also been shown to play an important role in host defense against pathogens by promoting the production of the human antimicrobial peptides, cathelicidins (LL-37).

• Human cathelicidin antimicrobial peptide (CAMP) gene is a direct target of the vitamin D receptor and is trongly up-regulated in myeloid cells by 1,25-dihydroxyvitamin D3

• On the Physiology and Pathophysiology of Antimicrobial Peptides

• Vitamin D as a defensin [in this case using defensin as a generic term for an endogenously synthesized antimicrobial agent]

These cathelicidins have been found to have broad spectrum antimicrobial activity, showing activity against the following microbes, among others:

• C. albicans

  Image: C. albicans treated with LL-37

• C. trachomatis
• Bacillus species (Several members)
• B. burgdorferi (Lyme Disease)
• E. coli

  Image: E. coli treated with LL-37 (Figure 10, Page 10)

• H. pylori
• M. tuberculosis
• Cytomegalovirus
• M. furfur & Dermatophyes (Seborrheic dermatitis and tinea infections)
• P. aeruginosa, S. aureus, S. epidermidis, Herpes simplex virus type 1, and Adenovirus
• Streptococcus species (Group A)

A couple of other important and apparently previously unrecognized functions of of the cathelicidins (LL-37) upregulated by Vitamin D3 are its effects on bacterial biofilm formation and eradication and its effects on secondary necrosisⁱ of neutrophils:

• The human host defence peptide LL-37 prevents bacterial biofilm formation.

• Effects of an LL-37-derived antimicrobial peptide in an animal model of biofilm Pseudomonas sinusitis

• Neutrophil secondary necrosis is induced by LL-37 derived from cathelicidin.

• Perspective: Solar ultraviolet-B irradiance and vitamin D may reduce the risk of septicemia

• Cathelicidins and functional analogues as antisepsis molecules.

While cathelicidins (LL-37) have been shown to have little or no direct effect against C. pnuemoniae, Vitamin D3 has been shown to disrupt the mechanism that the intracellularⁱi forms of C. pneumoniae use to prevent normal celluar apoptosisi, and it is believed that Vitamin D3 is active against the intracellularⁱ forms of C. pneumoniae through this mechanism:

• Vitamin D3 in Chlamydia pneumoniae Infection - Important effects on NF-kappaB and inhibitor of apoptosis proteins

The resulting die-off effects from Vitamin D3 can be quite large, and symptoms of secondary pophryia can also be dramatically increased. Vitamin D3 levels should therefore be increased very slowly when treating a C. pneumoniae infection!