2012年9月2日 訊 /生物谷BIOON/ --8月27日，刊登在國際雜志Journal of Clinical Investigation上的一項(xiàng)研究中,，來自俄勒岡州立大學(xué)的研究者揭示了煙酰胺,，即維生素B3或許可以應(yīng)對(duì)葡萄球菌感染引發(fā)的抗生素耐藥性。
研究者Adrian表示,，盡管研究結(jié)果非?？上玻墒俏覀?nèi)匀恍枰谂R床試驗(yàn)中進(jìn)行證明?？股厥且环N治療感染的特效藥,，但是其面臨的是細(xì)菌日益增長的耐藥性，尤其是金黃色葡萄球菌和銅綠假單胞菌的強(qiáng)烈的耐藥性,。
研究者發(fā)現(xiàn)臨床一定劑量的煙酰胺可以增加中性白細(xì)胞的數(shù)量和其效力,，而中性粒細(xì)胞是一種特定的血細(xì)胞，可以殺滅和吞噬致病菌,。目前并沒有證據(jù)指出,，正常飲食中或者維生素B3的額外添加對(duì)于抵御細(xì)菌感染有明顯的作用。
研究者在研究中發(fā)現(xiàn)煙酰胺的確可以打開機(jī)體某些抗微生物的基因,，使其表達(dá)來增加免疫細(xì)胞殺滅細(xì)菌的能力,。目前全世界最為嚴(yán)重和普遍的感染就是葡萄球菌的感染，主要為耐甲氧西林金黃色葡萄球菌感染,，其可以引發(fā)嚴(yán)重的威脅生命的感染，治療不及時(shí)可以導(dǎo)致患者死亡,。
研究者Liu表示,，我們很意外的發(fā)現(xiàn)維生素B3可以幫助機(jī)體抵御細(xì)菌的感染，這將會(huì)幫助降低細(xì)菌對(duì)于抗生素的耐藥性,。進(jìn)行臨床試驗(yàn)發(fā)現(xiàn),，臨床劑量的維生素B3可以在短短的幾小時(shí)之內(nèi)有效清除金黃色葡萄球菌的感染。（生物谷Bioon.com）
編譯自：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.
