Drug-resistant
gonorrhea, Neisseria gonorrhoeae (N. gonorrhoeae), is an emerging concern, especially because the risk of
bladder cancer is associated with this
infection. N. gonorrhoeae suppresses T-helper 1(Th1) and Th2 responses and enhances Th17 responses via a mechanism involving
transforming growth factor-beta (TGF-β) and regulatory T cells. Blockade of TGF-β alleviates the suppression of specific anti-gonococcal responses and allows Th1 and Th2 responses to emerge with concomitant boosting of immune memory and protective immunity.
Gonorrhea activates
nuclear factor kappaB (
NF-kappaB), which plays a critical role in signal-transduction pathways involved in
inflammation. The innate immune system can eventually clear
gonorrhea.
Vitamin D is emerging as a potential, powerful,
anti-microbial agent with these effects: it supports the innate immune system in combating
bacterial infections; it decreases levels of TGF-β and
NF-kappaB activation; and it induces production of
LL-37 (cathelicidin), which has antimicrobial and antiendotoxin properties. In addition, via an independent
vitamin D receptor pathway,
curcumin also induces LL-37 production, inhibiting N. gonorrhoeae-induced
NF-kappaB signaling and inducing autophagy. Therefore,
vitamin D and
curcumin taken together may be useful in combating both normal and drug-resistant
gonorrhea. Moreover, the possible synergy between these two agents in improving outcomes is worthy of additional investigation.