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    中科院PLoS解析菌血癥代謝組研究新發(fā)現(xiàn)

    【字體: 時(shí)間:2013年06月25日 來(lái)源:武漢物理與數(shù)學(xué)研究所

    編輯推薦:

      中國(guó)科學(xué)院生物磁共振分析重點(diǎn)實(shí)驗(yàn)室的生物醫(yī)學(xué)代謝組學(xué)研究組,在菌血癥的代謝組研究方面取得新進(jìn)展,相關(guān)研究結(jié)果發(fā)表在PLoS ONE上。

      

    近日,依托于中科院武漢物理與數(shù)學(xué)研究所的中國(guó)科學(xué)院生物磁共振分析重點(diǎn)實(shí)驗(yàn)室的生物醫(yī)學(xué)代謝組學(xué)研究組,在菌血癥的代謝組研究方面取得新進(jìn)展,相關(guān)研究結(jié)果發(fā)表在PLoS ONE上。

    菌血癥(bacteremia)是指外界的細(xì)菌經(jīng)由體表或感染的入口進(jìn)入血液系統(tǒng)內(nèi)繁殖并隨血流在全身播散,從而激發(fā)炎癥反應(yīng),導(dǎo)致全身炎癥反應(yīng)綜合征(systemic inflammatory response syndrome, SIRS)和多系統(tǒng)器官功能障礙綜合癥(multiple organ dysfunction syndrome,MODS)。鑒定與菌血癥有關(guān)的代謝產(chǎn)物并監(jiān)視其動(dòng)態(tài)變化有助于深入了解菌血癥的發(fā)生和發(fā)展機(jī)制,同時(shí)也為對(duì)該病進(jìn)行飲食干預(yù)提供了理論基礎(chǔ)。

    生物醫(yī)學(xué)代謝組學(xué)組董方聰博士,采用基于NMR的代謝組學(xué)方法并結(jié)合多變量數(shù)據(jù)分析手段,研究了宿主對(duì)肺炎克雷伯菌感染的菌血癥代謝應(yīng)答。發(fā)現(xiàn)肺炎克雷伯菌感染的菌血癥擾亂了機(jī)體的能量代謝,主要表現(xiàn)在促進(jìn)了糖酵解、三羧酸循環(huán),脂質(zhì)的氧化和磷酸肌酸的分解;誘導(dǎo)了宿主的抗細(xì)菌內(nèi)毒素,抗炎癥和抗氧化反應(yīng)。最后,菌血癥也導(dǎo)致宿主腸道菌群的紊亂。研究結(jié)果還表明,額外的補(bǔ)充葡萄糖和富含高脂和高膽堿的食物攝入可以有效地緩解菌血癥病人的病情。

    原文摘要:

    Metabolic Response to Klebsiella pneumoniae Infection in an Experimental Rat Model

    Bacteremia, the presence of viable bacteria in the blood stream, is often associated with several clinical conditions. Bacteremia can lead to multiple organ failure if managed incorrectly, which makes providing suitable nutritional support vital for reducing bacteremia-associated mortality. In order to provide such information, we investigated the metabolic consequences of a Klebsiella pneumoniae (K. pneumoniae) infection in vivo by employing a combination of 1H nuclear magnetic resonance spectroscopy and multivariate data analysis. K. pneumoniae was intravenously infused in rats; urine and plasma samples were collected at different time intervals. We found that K. pneumoniae-induced bacteremia stimulated glycolysis and the tricarboxylic acid cycle and also promoted oxidation of fatty acids and creatine phosphate to facilitate the energy-demanding host response. In addition, K. pneumoniae bacteremia also induced anti-endotoxin, anti-inflammatory and anti-oxidization responses in the host. Furthermore, bacteremia could cause a disturbance in the gut microbiotal functions as suggested by alterations in a range of amines and bacteria-host co-metabolites. Our results suggest that supplementation with glucose and a high-fat and choline-rich diet could ameliorate the burdens associated with bacteremia. Our research provides underlying pathological processes of bacteremia and a better understanding of the clinical and biochemical manifestations of bacteremia.

     

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