【medical-news】治疗常见院内感染有新招
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治疗常见院内感染有新招
译者：Docofsoul
《每日科学》2011年8月21日报道——加州大学洛杉矶分校（UCLA）大卫·格芬医学院与德州大学加尔维斯顿医学分校的研究者发现了人体抵御艰难梭菌感染（CDI）的分子过程，为近年来日趋普遍、严重、难愈的肠病提供了颇有前景的新的治疗方法。
左侧图片为正常结肠，右侧为结肠炎病理图片，显然右侧图片中巯基亚硝化水平（绿色）远比左侧高。（照片来源：UCLA与德州大学加尔维斯顿医学分校）
美国每年受感染的人数达数百万，即十年内翻了一番；其中的主要原因是可引起CDI的艰难梭菌出现了一种毒性很强的新菌株。本研究发表于8月21日《Nature Medicine》网络版，研究者眼下正着手启动以本发现作为新的CDI治疗方法的临床实验。研究小组包括来自凯斯西储大学、塔夫斯大学与联邦医学院的成员。
CDI是细菌感染的一种，可导致腹泻、结肠炎等肠症状，在最严重的情形下甚至可导致死亡。而且，CDI正是最常见的院内感染，尤其影响因其它感染而接受抗生素治疗的老年病人。目前应用两种强效抗生素中的一种来对抗CDI，但多达20%的病人在数周内即可复发，重新出现多种症状。
共同作者、UCLA炎性肠病中心主任、消化病学系医学教授Charalabos Pothoulakis博士说：“用另外一种抗生素来治疗因抗生素导致的疾病时，可使病人再次受到同一细菌的感染而产生多种症状。对新的CDI治疗方法的确定将是一项重大进步。”
艰难梭菌会向肠道释放两种强力毒素，毒素与肠上皮细胞结合后激发炎性反应而导致腹泻与结肠炎。但艰难梭菌在繁殖时才会释放毒素。当抗生素应用于治疗另外一种感染时，内脏中细菌的生态环境会为之改变，从而可能杀灭在正常情形下与艰难梭菌争夺能源的细菌。科学家相信，这一过程可能为艰难梭菌生长并释放毒素提供了机遇与条件。
UCLA与德州大学研究者在实验室研究中发现：感染艰难梭菌后，人类内脏细胞能够释放中和这些毒素的分子，使之无害化。在动物实验中，研究者显示，用药物诱导该蛋白巯基亚硝化（protein s-nitrosylation）过程可抑制艰难梭菌毒素，使之不再破坏肠细胞。进一步的临床实验将以人类患者为对象来测试这一方法。
论文第一作者、德州大学加尔维斯顿医学分校肠胃病学与肝病学系副教授Tor C. Savidge说：“研究提示，利用新发现的防卫机制（人类通过进化获得了这一机制，可使细菌毒素失去活性），可能获得治疗艰难梭菌感染的新方法。”
本发现除拥有为治疗CDI提供汲汲以求的新方法的潜力外，也可用于开发治疗其它形式腹泻以及由细胞导致的非腹泻性疾病的新疗法。
Pothoulakis说：“通过基因测序分析，目前已经了解数百种的细胞蛋白可为蛋白巯基亚硝化过程所调节。如果我们运用这一方法成功的话，就可能用相似的方式来治疗其它细菌性疾病。”
国立卫生研究所等（名单翻译从略）为本研究提供了资金。
论文的其他作者为（名单翻译从略）。
参考文献：
Tor C Savidge, Petri Urvil, Numan Oezguen, Kausar Ali, Aproteem Choudhury, Vinay Acharya, Irina Pinchuk, Alfredo G Torres, Robert D English, John E Wiktorowicz, Michael Loeffelholz, Raj Kumar, Lianfa Shi, Weijia Nie, Werner Braun, Bo Herman, Alfred Hausladen, Hanping Feng, Jonathan S Stamler, Charalabos Pothoulakis. Host S-nitrosylation inhibits clostridial small molecule–activated glucosylating toxins. Nature Medicine, 2011; DOI: 10.1038/nm.2405
http://www.sciencedaily.com/releases/2011/08/110821141128.htm
Docofsoul译于2011-8-22
译后中文字数为１０３８个。
==================================================
New Way to Treat Common Hospital-Acquired Infection: Novel Approach May Offer Treatment for Other Bacterial Diseases
治疗常见院内感染有新招
译者：Docofsoul
ScienceDaily (Aug. 21, 2011)— Researchers at the David Geffen School of Medicine at UCLA and the University of Texas Medical Branch at Galveston have discovered a molecular process by which the body can defend against the effects of Clostridium difficile infection (CDI), pointing the way to a promising new approach for treating an intestinal disease that has become more common, more severe and harder to cure in recent years.
《每日科学》2011年8月21日报道——加州大学洛杉矶分校（UCLA）大卫·格芬医学院与德州大学加尔维斯顿医学分校的研究者发现了人体抵御艰难梭菌感染（CDI）的分子过程，为近年来日趋普遍、严重、难愈的肠病提供了颇有前景的新的治疗方法。
The right image shows abundant S-nitrosylation (green) in human colitis compared with much less found in the left image of a normal colon. (Credit: UCLA/University of Texas Medical Branch at Galveston)
左侧图片为正常结肠，右侧为结肠炎病理图片，显然右侧图片中巯基亚硝化水平（绿色）远比左侧高。
In the U.S., several million people are infected each year, approximately double the incidence of a decade ago, mainly due to the emergence of a new, highly virulent strain of the bacteria that causes CDI.
As a result of the study findings, published in the Aug. 21 online edition of the journal Nature Medicine, the researchers are preparing to launch clinical trials using their discovery as a new CDI therapeutic approach. The team also included researchers from Case Western Reserve University, Tufts University and the Commonwealth Medical College.
美国每年受感染的人数达数百万，即十年内翻了一番；其中的主要原因是可引起CDI的艰难梭菌出现了一种毒性很强的新菌株。本研究发表于8月21日《Nature Medicine》网络版，研究者眼下正着手启动以本发现作为新的CDI治疗方法的临床实验。研究小组包括来自凯斯西储大学、塔夫斯大学与联邦医学院的成员。
CDI is a bacterial infection that can cause diarrhea and more serious intestinal conditions, such as colitis, the inflammation of the colon. In the most severe cases, CDI can be fatal. It is most commonly acquired in hospitals by patients, particularly the elderly, who are being treated with antibiotics for another infection.
Currently, one of two potent antibiotics is used to treat the infection, but up to 20 percent of patients experience a relapse and a return of symptoms within a few weeks.
CDI是细菌感染的一种，可导致腹泻、结肠炎等肠症状，在最严重的情形下甚至可导致死亡。而且，CDI正是最常见的院内感染，尤其影响因其它感染而接受抗生素治疗的老年病人。目前应用两种强效抗生素中的一种来对抗CDI，但多达20%的病人在数周内即可复发，重新出现多种症状。
"We are treating a disease caused by antibiotics with yet another antibiotic, which creates the conditions for re-infection from the same bacteria," said study co-author Dr. Charalabos Pothoulakis, director of UCLA's Inflammatory Bowel Disease Center and a professor of medicine in the division of digestive diseases. "Identification of new treatment modalities to treat this infection would be a major advance."
共同作者、UCLA炎性肠病中心主任、消化病学系医学教授Charalabos Pothoulakis博士说：“用另外一种抗生素来治疗因抗生素导致的疾病时，可使病人再次受到同一细菌的感染而产生多种症状。对新的CDI治疗方法的确定将是一项重大进步。”
Clostridium difficilecauses diarrhea and colitis by releasing two potent toxins into the gut lumen that bind to intestinal epithelial cells, initiating an inflammatory response. These toxins are released only when the Clostridium difficile bacteria are multiplying. When antibiotics are used to treat another infection, it changes the bacterial landscape in the gut and, in the process, may kill bacteria that under normal conditions would compete with Clostridium difficile for energy. Scientists believe this may be what provides the opportunity for Clostridium difficile to grow and release its toxins.
艰难梭菌会向肠道释放两种强力毒素，毒素与肠上皮细胞结合后激发炎性反应而导致腹泻与结肠炎。但艰难梭菌在繁殖时才会释放毒素。当抗生素应用于治疗另外一种感染时，内脏中细菌的生态环境会为之改变，从而可能杀灭在正常情形下与艰难梭菌争夺能源的细菌。科学家相信，这一过程可能为艰难梭菌生长并释放毒素提供了机遇与条件。
The UCLA and University of Texas researchers found in laboratory studies that upon infection with Clostridium difficile, human cells in the gut are capable of releasing molecules that will neutralize these toxins, rendering them harmless. In animal studies, the researchers showed that using a drug to induce this process, known as protein s-nitrosylation, inhibited Clostridium difficile toxins from destroying intestinal cells. Forthcoming clinical trials will test this approach in humans.
UCLA与德州大学研究者在实验室研究中发现：感染艰难梭菌后，人类内脏细胞能够释放中和这些毒素的分子，使之无害化。在动物实验中，研究者显示，用药物诱导该蛋白巯基亚硝化（protein s-nitrosylation）过程可抑制艰难梭菌毒素，使之不再破坏肠细胞。进一步的临床实验将以人类患者为对象来测试这一方法。
"Our study suggests a novel therapeutic approach for treating Clostridium difficile infection by exploiting a newly discovered defense mechanism that has evolved in humans to inactivate microbial toxins," said Tor C. Savidge, an associate professor in the division of gastroenterology and hepatology at the University of Texas Medical Branch at Galveston and the paper's lead author.
论文第一作者、德州大学加尔维斯顿医学分校肠胃病学与肝病学系副教授Tor C. Savidge说：“研究提示，利用新发现的防卫机制（人类通过进化获得了这一机制，可使细菌毒素失去活性），可能获得治疗艰难梭菌感染的新方法。”
Along with its potential to provide a much-needed new approach to treating CDI, the discovery could be applied to developing new treatments for other forms of diarrhea, as well as non-diarrheal diseases caused by bacteria.
本发现除拥有为治疗CDI提供汲汲以求的新方法的潜力外，也可用于开发治疗其它形式腹泻以及由细胞导致的非腹泻性疾病的新疗法。
"We already know through gene-sequencing analysis that hundreds of microbial proteins can be regulated by s-nitrosylation," Pothoulakis said. "If we are successful with this approach, we may be able to treat other bacterial diseases in a similar way."
Pothoulakis说：“通过基因测序分析，目前已经了解数百种的细胞蛋白可为蛋白巯基亚硝化过程所调节。如果我们运用这一方法成功的话，就可能用相似的方式来治疗其它细菌性疾病。”
The study was funded by grants from the National Institutes of Health, The Eli and Edythe Broad Medical Foundation, the John S. Dunn Gulf Coast Consortium for Chemical Genomics/Robert A. Welch Collaborative Grant Program, and the Howard Hughes Medical Institute.
国立卫生研究所等（名单翻译从略）为本研究提供了资金。
Other study authors included Petri Urvil, Numan Oezguen, Ali Kausar, Aproteem Choudhury, Vinay Acharya, Irina Pinchuk, Alfredo G. Torres, Robert D. English, Michael Loeffelholz and Werner Braun from the University of Texas Medical Branch at Galveston; Raj Kumar from the Commonwealth Medical College; Liamfa Shi, Weijia Nie and Hanping Feng from Tufts University; and Bo Herman, Alfred Hausladen and Jonathan S. Stamier from Case Western Reserve University.
论文的其他作者为（名单翻译从略）。
Journal Reference:
参考文献：
Tor C Savidge, Petri Urvil, Numan Oezguen, Kausar Ali, Aproteem Choudhury, Vinay Acharya, Irina Pinchuk, Alfredo G Torres, Robert D English, John E Wiktorowicz, Michael Loeffelholz, Raj Kumar, Lianfa Shi, Weijia Nie, Werner Braun, Bo Herman, Alfred Hausladen, Hanping Feng, Jonathan S Stamler, Charalabos Pothoulakis. Host S-nitrosylation inhibits clostridial small molecule–activated glucosylating toxins. Nature Medicine, 2011; DOI: 10.1038/nm.2405
http://www.sciencedaily.com/releases/2011/08/110821141128.htm
Docofsoul译于2011-8-22
译后中文字数为１０３８个。
译者：Docofsoul
《每日科学》2011年8月21日报道——加州大学洛杉矶分校（UCLA）大卫·格芬医学院与德州大学加尔维斯顿医学分校的研究者发现了人体抵御艰难梭菌感染（CDI）的分子过程，为近年来日趋普遍、严重、难愈的肠病提供了颇有前景的新的治疗方法。
左侧图片为正常结肠，右侧为结肠炎病理图片，显然右侧图片中巯基亚硝化水平（绿色）远比左侧高。（照片来源：UCLA与德州大学加尔维斯顿医学分校）
美国每年受感染的人数达数百万，即十年内翻了一番；其中的主要原因是可引起CDI的艰难梭菌出现了一种毒性很强的新菌株。本研究发表于8月21日《Nature Medicine》网络版，研究者眼下正着手启动以本发现作为新的CDI治疗方法的临床实验。研究小组包括来自凯斯西储大学、塔夫斯大学与联邦医学院的成员。
CDI是细菌感染的一种，可导致腹泻、结肠炎等肠症状，在最严重的情形下甚至可导致死亡。而且，CDI正是最常见的院内感染，尤其影响因其它感染而接受抗生素治疗的老年病人。目前应用两种强效抗生素中的一种来对抗CDI，但多达20%的病人在数周内即可复发，重新出现多种症状。
共同作者、UCLA炎性肠病中心主任、消化病学系医学教授Charalabos Pothoulakis博士说：“用另外一种抗生素来治疗因抗生素导致的疾病时，可使病人再次受到同一细菌的感染而产生多种症状。对新的CDI治疗方法的确定将是一项重大进步。”
艰难梭菌会向肠道释放两种强力毒素，毒素与肠上皮细胞结合后激发炎性反应而导致腹泻与结肠炎。但艰难梭菌在繁殖时才会释放毒素。当抗生素应用于治疗另外一种感染时，内脏中细菌的生态环境会为之改变，从而可能杀灭在正常情形下与艰难梭菌争夺能源的细菌。科学家相信，这一过程可能为艰难梭菌生长并释放毒素提供了机遇与条件。
UCLA与德州大学研究者在实验室研究中发现：感染艰难梭菌后，人类内脏细胞能够释放中和这些毒素的分子，使之无害化。在动物实验中，研究者显示，用药物诱导该蛋白巯基亚硝化（protein s-nitrosylation）过程可抑制艰难梭菌毒素，使之不再破坏肠细胞。进一步的临床实验将以人类患者为对象来测试这一方法。
论文第一作者、德州大学加尔维斯顿医学分校肠胃病学与肝病学系副教授Tor C. Savidge说：“研究提示，利用新发现的防卫机制（人类通过进化获得了这一机制，可使细菌毒素失去活性），可能获得治疗艰难梭菌感染的新方法。”
本发现除拥有为治疗CDI提供汲汲以求的新方法的潜力外，也可用于开发治疗其它形式腹泻以及由细胞导致的非腹泻性疾病的新疗法。
Pothoulakis说：“通过基因测序分析，目前已经了解数百种的细胞蛋白可为蛋白巯基亚硝化过程所调节。如果我们运用这一方法成功的话，就可能用相似的方式来治疗其它细菌性疾病。”
国立卫生研究所等（名单翻译从略）为本研究提供了资金。
论文的其他作者为（名单翻译从略）。
参考文献：
Tor C Savidge, Petri Urvil, Numan Oezguen, Kausar Ali, Aproteem Choudhury, Vinay Acharya, Irina Pinchuk, Alfredo G Torres, Robert D English, John E Wiktorowicz, Michael Loeffelholz, Raj Kumar, Lianfa Shi, Weijia Nie, Werner Braun, Bo Herman, Alfred Hausladen, Hanping Feng, Jonathan S Stamler, Charalabos Pothoulakis. Host S-nitrosylation inhibits clostridial small molecule–activated glucosylating toxins. Nature Medicine, 2011; DOI: 10.1038/nm.2405
http://www.sciencedaily.com/releases/2011/08/110821141128.htm
Docofsoul译于2011-8-22
译后中文字数为１０３８个。
==================================================
New Way to Treat Common Hospital-Acquired Infection: Novel Approach May Offer Treatment for Other Bacterial Diseases
治疗常见院内感染有新招
译者：Docofsoul
ScienceDaily (Aug. 21, 2011)— Researchers at the David Geffen School of Medicine at UCLA and the University of Texas Medical Branch at Galveston have discovered a molecular process by which the body can defend against the effects of Clostridium difficile infection (CDI), pointing the way to a promising new approach for treating an intestinal disease that has become more common, more severe and harder to cure in recent years.
《每日科学》2011年8月21日报道——加州大学洛杉矶分校（UCLA）大卫·格芬医学院与德州大学加尔维斯顿医学分校的研究者发现了人体抵御艰难梭菌感染（CDI）的分子过程，为近年来日趋普遍、严重、难愈的肠病提供了颇有前景的新的治疗方法。
The right image shows abundant S-nitrosylation (green) in human colitis compared with much less found in the left image of a normal colon. (Credit: UCLA/University of Texas Medical Branch at Galveston)
左侧图片为正常结肠，右侧为结肠炎病理图片，显然右侧图片中巯基亚硝化水平（绿色）远比左侧高。
In the U.S., several million people are infected each year, approximately double the incidence of a decade ago, mainly due to the emergence of a new, highly virulent strain of the bacteria that causes CDI.
As a result of the study findings, published in the Aug. 21 online edition of the journal Nature Medicine, the researchers are preparing to launch clinical trials using their discovery as a new CDI therapeutic approach. The team also included researchers from Case Western Reserve University, Tufts University and the Commonwealth Medical College.
美国每年受感染的人数达数百万，即十年内翻了一番；其中的主要原因是可引起CDI的艰难梭菌出现了一种毒性很强的新菌株。本研究发表于8月21日《Nature Medicine》网络版，研究者眼下正着手启动以本发现作为新的CDI治疗方法的临床实验。研究小组包括来自凯斯西储大学、塔夫斯大学与联邦医学院的成员。
CDI is a bacterial infection that can cause diarrhea and more serious intestinal conditions, such as colitis, the inflammation of the colon. In the most severe cases, CDI can be fatal. It is most commonly acquired in hospitals by patients, particularly the elderly, who are being treated with antibiotics for another infection.
Currently, one of two potent antibiotics is used to treat the infection, but up to 20 percent of patients experience a relapse and a return of symptoms within a few weeks.
CDI是细菌感染的一种，可导致腹泻、结肠炎等肠症状，在最严重的情形下甚至可导致死亡。而且，CDI正是最常见的院内感染，尤其影响因其它感染而接受抗生素治疗的老年病人。目前应用两种强效抗生素中的一种来对抗CDI，但多达20%的病人在数周内即可复发，重新出现多种症状。
"We are treating a disease caused by antibiotics with yet another antibiotic, which creates the conditions for re-infection from the same bacteria," said study co-author Dr. Charalabos Pothoulakis, director of UCLA's Inflammatory Bowel Disease Center and a professor of medicine in the division of digestive diseases. "Identification of new treatment modalities to treat this infection would be a major advance."
共同作者、UCLA炎性肠病中心主任、消化病学系医学教授Charalabos Pothoulakis博士说：“用另外一种抗生素来治疗因抗生素导致的疾病时，可使病人再次受到同一细菌的感染而产生多种症状。对新的CDI治疗方法的确定将是一项重大进步。”
Clostridium difficilecauses diarrhea and colitis by releasing two potent toxins into the gut lumen that bind to intestinal epithelial cells, initiating an inflammatory response. These toxins are released only when the Clostridium difficile bacteria are multiplying. When antibiotics are used to treat another infection, it changes the bacterial landscape in the gut and, in the process, may kill bacteria that under normal conditions would compete with Clostridium difficile for energy. Scientists believe this may be what provides the opportunity for Clostridium difficile to grow and release its toxins.
艰难梭菌会向肠道释放两种强力毒素，毒素与肠上皮细胞结合后激发炎性反应而导致腹泻与结肠炎。但艰难梭菌在繁殖时才会释放毒素。当抗生素应用于治疗另外一种感染时，内脏中细菌的生态环境会为之改变，从而可能杀灭在正常情形下与艰难梭菌争夺能源的细菌。科学家相信，这一过程可能为艰难梭菌生长并释放毒素提供了机遇与条件。
The UCLA and University of Texas researchers found in laboratory studies that upon infection with Clostridium difficile, human cells in the gut are capable of releasing molecules that will neutralize these toxins, rendering them harmless. In animal studies, the researchers showed that using a drug to induce this process, known as protein s-nitrosylation, inhibited Clostridium difficile toxins from destroying intestinal cells. Forthcoming clinical trials will test this approach in humans.
UCLA与德州大学研究者在实验室研究中发现：感染艰难梭菌后，人类内脏细胞能够释放中和这些毒素的分子，使之无害化。在动物实验中，研究者显示，用药物诱导该蛋白巯基亚硝化（protein s-nitrosylation）过程可抑制艰难梭菌毒素，使之不再破坏肠细胞。进一步的临床实验将以人类患者为对象来测试这一方法。
"Our study suggests a novel therapeutic approach for treating Clostridium difficile infection by exploiting a newly discovered defense mechanism that has evolved in humans to inactivate microbial toxins," said Tor C. Savidge, an associate professor in the division of gastroenterology and hepatology at the University of Texas Medical Branch at Galveston and the paper's lead author.
论文第一作者、德州大学加尔维斯顿医学分校肠胃病学与肝病学系副教授Tor C. Savidge说：“研究提示，利用新发现的防卫机制（人类通过进化获得了这一机制，可使细菌毒素失去活性），可能获得治疗艰难梭菌感染的新方法。”
Along with its potential to provide a much-needed new approach to treating CDI, the discovery could be applied to developing new treatments for other forms of diarrhea, as well as non-diarrheal diseases caused by bacteria.
本发现除拥有为治疗CDI提供汲汲以求的新方法的潜力外，也可用于开发治疗其它形式腹泻以及由细胞导致的非腹泻性疾病的新疗法。
"We already know through gene-sequencing analysis that hundreds of microbial proteins can be regulated by s-nitrosylation," Pothoulakis said. "If we are successful with this approach, we may be able to treat other bacterial diseases in a similar way."
Pothoulakis说：“通过基因测序分析，目前已经了解数百种的细胞蛋白可为蛋白巯基亚硝化过程所调节。如果我们运用这一方法成功的话，就可能用相似的方式来治疗其它细菌性疾病。”
The study was funded by grants from the National Institutes of Health, The Eli and Edythe Broad Medical Foundation, the John S. Dunn Gulf Coast Consortium for Chemical Genomics/Robert A. Welch Collaborative Grant Program, and the Howard Hughes Medical Institute.
国立卫生研究所等（名单翻译从略）为本研究提供了资金。
Other study authors included Petri Urvil, Numan Oezguen, Ali Kausar, Aproteem Choudhury, Vinay Acharya, Irina Pinchuk, Alfredo G. Torres, Robert D. English, Michael Loeffelholz and Werner Braun from the University of Texas Medical Branch at Galveston; Raj Kumar from the Commonwealth Medical College; Liamfa Shi, Weijia Nie and Hanping Feng from Tufts University; and Bo Herman, Alfred Hausladen and Jonathan S. Stamier from Case Western Reserve University.
论文的其他作者为（名单翻译从略）。
Journal Reference:
参考文献：
Tor C Savidge, Petri Urvil, Numan Oezguen, Kausar Ali, Aproteem Choudhury, Vinay Acharya, Irina Pinchuk, Alfredo G Torres, Robert D English, John E Wiktorowicz, Michael Loeffelholz, Raj Kumar, Lianfa Shi, Weijia Nie, Werner Braun, Bo Herman, Alfred Hausladen, Hanping Feng, Jonathan S Stamler, Charalabos Pothoulakis. Host S-nitrosylation inhibits clostridial small molecule–activated glucosylating toxins. Nature Medicine, 2011; DOI: 10.1038/nm.2405
http://www.sciencedaily.com/releases/2011/08/110821141128.htm
Docofsoul译于2011-8-22
译后中文字数为１０３８个。
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