Journal
MEDICAL HYPOTHESES
Volume 81, Issue 1, Pages 131-135Publisher
CHURCHILL LIVINGSTONE
DOI: 10.1016/j.mehy.2013.04.013
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Funding
- Bio-Tech Pharmacal (Fayetteville, AR)
- Sunlight Research Forum (Veldhoven)
- UV Foundation (McLean, VA)
- Vitamin D Council (San Luis Obispo, CA)
- Vitamin D Society (Canada)
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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-beta) and regulatory T cells. Blockade of TGF-beta 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-beta 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. (C) 2013 Elsevier Ltd. All rights reserved.
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