为什么对抗生素有抵抗力的细菌在感染接受抗生素治疗的患者时非常成功？这是一个有点儿神秘的问题。本期Nature报告了一个以前未被发现的因素：用广谱抗生素万古霉素治疗，会因为削弱小肠先天免疫力而增加有抵抗力的细菌所造成的感染。
在接受该抗生素的小鼠中，抗菌蛋白RegIIIγ在小肠的表达被抑制。RegIIIγ对于治疗对万古霉素有抵抗力的细菌肠球菌（Enterococcus (VRE)）所造成的感染疗效显著，该细菌是造成住院患者感染的一个常见原因。因此，能够提高这种蛋白水平的疗法（如口服脂多糖）也许可用于接受广谱抗生素治疗的患者。（生物谷Bioon.com）
生物谷推荐原始出处：
Nature 455, 804-807 (9 October 2008) | doi:10.1038/nature07250
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
1 Infectious Diseases Service, Department of Medicine, Immunology Program, Sloan-Kettering Institute
2 Hepatobiliary Service,
3 Department of Clinical Laboratories, Memorial Sloan-Kettering Cancer Center, 1275 York Avenue, New York, New York 10021, USA
4 Department of Medicine, Columbia University, New York, New York 10032, USA
5 Present addresses: 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, 1515 Holcombe Boulevard, Houston, Texas 77030, USA (C.N.M.); Department of Medicine, University of California San Diego, La Jolla, California 92093, USA (B.S.).
Infection with antibiotic-resistant bacteria, such as vancomycin-resistantEnterococcus (VRE), is a dangerous and costly complication of broad-spectrum antibiotic therapy1, 2. How antibiotic-mediated elimination of commensal bacteria promotes infection by antibiotic-resistant bacteria is a fertile area for speculation with few defined mechanisms. Here we demonstrate that antibiotic treatment of mice notably downregulates intestinal expression of RegIIIγ (also known as Reg3g), a secreted C-type lectin that kills Gram-positive bacteria, including VRE. Downregulation of RegIIIγ markedly decreases in vivo killing of VRE in the intestine of antibiotic-treated mice. Stimulation of intestinal Toll-like receptor 4 by oral administration of lipopolysaccharide re-induces RegIIIγ, thereby boosting innate immune resistance of antibiotic-treated mice against VRE. Compromised mucosal innate immune defence, as induced by broad-spectrum antibiotic therapy, can be corrected by selectively stimulating mucosal epithelial Toll-like receptors, providing a potential therapeutic approach to reduce colonization and infection by antibiotic-resistant microbes.
