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Protection of Immuno-Compromised Mice from Lethal Infection of Klebsiella pneumonia by rAAV2-BPI23-Fcγ1 Gene Transfer

Protection of Immuno-Compromised Mice from Lethal Infection of Klebsiella pneumonia by rAAV2-BPI23-Fcγ1 Gene Transfer

作     者:Jing Li Qingli Kong Zhe Lv Yuanzhi Guan Yong Qiu Chen Li Mingjie Sun Zhenlong Liu Yunqing An 

作者机构:Department of Immunology Capital Medical University Beijing 100069China Laboratory Department Capital Institute of Pediatrics Beijing 100020China Department of Microbiology Institute of Basic Medical Sciences ChineseAcademy of Medical Sciences & Peking Union Medical College Beijing100005 China Laboratory Department Beijing Shijitan Hospital Beijing 100038 China China Rehabilitation Center Institute of Medical Sciences Beijing 100077China 

出 版 物:《Cellular & Molecular Immunology》 (中国免疫学杂志(英文版))

年 卷 期:2008年第5卷第6期

页      面:439-445页

核心收录:

学科分类:0710[理学-生物学] 1004[医学-公共卫生与预防医学(可授医学、理学学位)] 1002[医学-临床医学] 1001[医学-基础医学(可授医学、理学学位)] 100201[医学-内科学(含:心血管病、血液病、呼吸系病、消化系病、内分泌与代谢病、肾病、风湿病、传染病)] 10[医学] 

基  金:funded by the Beijing Municipal Natural Science Foundation (7082016) 

主  题:rAAV2 BPI immuno-compromised mouse Klebsiella pneumonia gene transfer 

摘      要:In previous research, chimerical BPI23-Fcy1 gene which consisted of human bactericidal/permeability increasing protein (BPI) gene of encoding the functional N terminus (amino acid residues 1 to 199) of human BPI and Fcy1 gene of encoding the Fc segment of human immunoglobulin G1 was successfully reconstructed within a recombinant adeno-associated virus serotype 2 (rAAV2) vector as rAAV2-BPI23-Fcy1. Here, to evaluate the potentiality of applying gene therapy to gram negative bacterial (GNB) infection in high-risk patients, we investigated protection of immuno-compromised mice and immunocompetent mice from challenge with minimal lethal dose (MLD) Klebsiella pneumonia infection after rAAV2-BPI23-Fcy1 gene transferred. The results showed that the survival rate of rAAV2-BPI23-Fcy1 transferred immunocompetent mice as well as immuno-compromised mice (40.0% and 44.4%, respectively) were significant higher than that of corresponding control mice (6.7% and 4.4%, respectively); the bacteria counting, level of endotoxin and proinflammatory cytokines in the rAAV2-BP123-Fcy1 transferred immuno-compromised mice were markedly lower than that of rAAV2-EGFP and rAAV2-Null transferred immuno- compromised mice. Our data suggest that rAAV2-BPI23-Fcy1 gene transferring offered immuno-compromised mice with resistance against GNB infection, so it is quite potential in preventing GNB infection of clinical high-risk patients. Cellular & Molecular Immunology. 2008;5(6):439-445.

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