2012年9月2日 讯 /生物谷BIOON/ --8月27日，刊登在国际杂志Journal of Clinical Investigation上的一项研究中，来自俄勒冈州立大学的研究者揭示了烟酰胺，即维生素B3或许可以应对葡萄球菌感染引发的抗生素耐药性。
研究者Adrian表示，尽管研究结果非常可喜，可是我们仍然需要在临床试验中进行证明。抗生素是一种治疗感染的特效药，但是其面临的是细菌日益增长的耐药性，尤其是金黄色葡萄球菌和铜绿假单胞菌的强烈的耐药性。
研究者发现临床一定剂量的烟酰胺可以增加中性白细胞的数量和其效力，而中性粒细胞是一种特定的血细胞，可以杀灭和吞噬致病菌。目前并没有证据指出，正常饮食中或者维生素B3的额外添加对于抵御细菌感染有明显的作用。
研究者在研究中发现烟酰胺的确可以打开机体某些抗微生物的基因，使其表达来增加免疫细胞杀灭细菌的能力。目前全世界最为严重和普遍的感染就是葡萄球菌的感染，主要为耐甲氧西林金黄色葡萄球菌感染，其可以引发严重的威胁生命的感染，治疗不及时可以导致患者死亡。
研究者Liu表示，我们很意外的发现维生素B3可以帮助机体抵御细菌的感染，这将会帮助降低细菌对于抗生素的耐药性。进行临床试验发现，临床剂量的维生素B3可以在短短的几小时之内有效清除金黄色葡萄球菌的感染。（生物谷Bioon.com）
编译自：Vitamin B3 May Offer New Tool in Fight Against Staph Infections, 'Superbugs'
doi:10.1172/JCI62070
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C/EBPε mediates nicotinamide-enhanced clearance of Staphylococcus aureus in mice
Pierre Kyme1,2,3, Nils H. Thoennissen4,5, Ching Wen Tseng1,2,3, Gabriela B. Thoennissen4,5, Andrea J. Wolf2, Kenichi Shimada1,2,3, Utz O. Krug5, Kunik Lee4, Carsten Müller-Tidow5, Wolfgang E. Berdel5, W. David Hardy6, Adrian F. Gombart7, H. Phillip Koeffler4,8 and George Y. Liu1,2,3
The myeloid-specific transcription factor, CCAAT/enhancer-binding protein ε (C/EBPε) is a critical mediator of myelopoiesis. Mutation of this gene is responsible for neutrophil-specific granule deficiency in humans, a condition that confers susceptibility to Staphylococcus aureus infection. We found that C/EBPε-deficient mice are severely affected by infection with S. aureus, and C/EBPε deficiency in neutrophils contributes to the infectious phenotype. Conversely, exposure to the epigenetic modulator nicotinamide (vitamin B3) increased expression of C/EBPε in WT myeloid cells. Further, nicotinamide increased the activity of C/EBPε and select downstream antimicrobial targets, particularly in neutrophils. In a systemic murine infection model as well as in murine and human peripheral blood, nicotinamide enhanced killing of S. aureus by up to 1,000 fold but had no effect when administered to either C/EBPε-deficient mice or mice depleted of neutrophils. Nicotinamide was efficacious in both prophylactic and therapeutic settings. Our findings suggest that C/EBPε is an important target to boost killing of bacteria by the innate immune system.
