Submitted by Red on Sat, 2009-02-21 14:47

 Studies have shown that Cpn inhibits apoptosis by interfering with with cytochrome c release and caspase activation:

 Studies also suggest that Vitamin D3, or more specifically, the antimicrobial peptides, cathelicidins (LL-37)  induces apoptosis of  infected cells "via enhanced LL-37-induced mitochondrial membrane depolarisation and release of cytochrome c, with activation of caspases -9 and -3":

   Studies also suggest that Cpni interferes with NF-KappaB regulation via "degradation of BH3-only proteins such as Bim, Puma, Bad, Bik, Bmf, Noxa, and tBid, which inhibit proapoptotic Bax and Bak.":

The following study seems to go one step further and suggests that in Cpn: "Persistent infection resulted in the upregulation of the NF-kappaB regulated inhibitor of apoptosisi protein 2 (cIAP-2) but not inhibitor of apoptosis protein 1 (cIAP-1)".  However, the study also suggests "silencing of either cIAP-1 or cIAP-2 sensitized infected cells [or causes apoptosis in other words, I believe] suggesting that IAPs play an important role in the apoptosis resistance of persistently infected cells":

 Apparently this action occurs directly through Vitamin D Receptors (VDRs) on numerous cell types in the body.   Here are a few articles discussing VDR signalling and NF-KappaB activation in various cell types:

 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! It is also through its effects on NF-KappaB, that Vitamin D is believed to play a beneficial role in the prevention of and potentially treatment of, cancers: