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

• Characterization of Antiapoptotic Activities of Chlamydia pneumoniae in Human Cells<

• Inhibition of apoptosis in neuronal cells infected with Chlamydophila (Chlamydia) pneumoniae<

• Chlamydia pneumoniae multiply in neutrophil granulocytes and delay their spontaneous apoptosis<

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":

• The Human Cathelicidin LL-37 Preferentially Promotes Apoptosis of Infected Airway Epithelium <

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.":

• Chlamydia Inhibit Host Cell Apoptosis by Degradation of Proapoptotic BH3-only Proteins<

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":

• NF-kappaB and inhibitor of apoptosis proteins are required for apoptosis resistance of epithelial cells persistently infected with Chlamydophila pneumoniae<

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:

• 20-Hydroxycholecalciferol, Product of Vitamin D3 Hydroxylation by P450scc, Decreases NF-κB Activity by Increasing IκBα Levels in Human Keratinocytes<

• Increased NF-kappaB activity in fibroblasts lacking the vitamin D receptor.<

• Involvement of different nuclear hormone receptors in butyrate-mediated inhibition of inducible NF kappa B signalling.<

• Involvement of different nuclear hormone receptors in butyrate-mediated inhibition of inducible NF kappa B signalling.<

• Vitamin D and the hematolymphopoietic tissue: a 1994 update<

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:

• Apoptosis Induction by 1,25-Dihydroxyvitamin D₃ in Prostate Cancer<