神马文学网Nature：抗生素可破坏肠道先天免疫力 - 生物研究-生物谷
来源：百度文库 编辑：神马文学网 时间：2024/04/28 06:23:07
日前发表在英国《自然》（ Nature ）周刊上的一篇文章指出，使用抗生素有可能破坏肠道的先天免疫力，这也是引起耐抗生素细菌感染的原因。
研究人员对耐抗生素细菌感染原因进行了研究，这是一种广泛使用抗生素导致的并发症，将使住院治疗患者的身体健康受到更大的伤害。
研究发现，尽管抗生素能够消灭肠道中的很多细菌，但由抗生素治疗引起的肠道先天免疫功能的损伤也为耐抗生素细菌的繁殖提供了温床。
研究人员在观察实验鼠接受抗生素治疗后的反应时，在其体内发现了少量能够抵抗微生物的肠蛋白RegⅢ伽马。这种肠蛋白能够消灭耐万古霉素肠球菌等高耐抗生素性细菌。
据此，科学家主张研发能够提高肠内RegⅢ伽马蛋白含量的疗法，以避免因使用抗生素而导致的细菌感染。（生物谷Bioon.com）
生物谷推荐原始出处：
Nature ，doi:10.1038/nature07250，Katharina Brandl, Eric G. Pamer
Vancomycin-resistant enterococci exploit antibiotic-induced innate immune deficits
Katharina Brandl1,5, George Plitas2, Coralia N. Mihu1,5, Carles Ubeda1, Ting Jia1, Martin Fleisher3, Bernd Schnabl4,5, Ronald P. DeMatteo2 & Eric G. Pamer1,3
Infectious Diseases Service, Department of Medicine, Immunology Program, Sloan-Kettering Institute
Hepatobiliary Service,
Department of Clinical Laboratories, Memorial Sloan-Kettering Cancer Center, 1275 York Avenue, New York, New York 10021, USA
Department of Medicine, Columbia University, New York, New York 10032, USA
Presentaddresses: Department of Genetics, The Scripps Research Institute,10550 North Torrey Pines Road, La Jolla, California 92037, USA (K.B.);Department of Infectious Diseases, MD Anderson Cancer Center, 1515Holcombe Boulevard, Houston, Texas 77030, USA (C.N.M.); Department ofMedicine, University of California San Diego, La Jolla, California92093, USA (B.S.).
Infection with antibiotic-resistant bacteria, such as vancomycin-resistant Enterococcus (VRE), is a dangerous and costly complication of broad-spectrum antibiotic therapy1, 2.How antibiotic-mediated elimination of commensal bacteria promotesinfection by antibiotic-resistant bacteria is a fertile area forspeculation with few defined mechanisms. Here we demonstrate thatantibiotic treatment of mice notably downregulates intestinal expressionof RegIII
(also known as Reg3g), a secreted C-type lectin that kills Gram-positive bacteria, including VRE. Downregulation of RegIII markedly decreases in vivokilling of VRE in the intestine of antibiotic-treated mice. Stimulationof intestinal Toll-like receptor 4 by oral administration oflipopolysaccharide re-induces RegIII,thereby boosting innate immune resistance of antibiotic-treated miceagainst VRE. Compromised mucosal innate immune defence, as induced bybroad-spectrum antibiotic therapy, can be corrected by selectivelystimulating mucosal epithelial Toll-like receptors, providing apotential therapeutic approach to reduce colonization and infection byantibiotic-resistant microbes.