為什么對抗生素有抵抗力的細(xì)菌在感染接受抗生素治療的患者時非常成功,？這是一個有點(diǎn)兒神秘的問題,。本期Nature報告了一個以前未被發(fā)現(xiàn)的因素：用廣譜抗生素萬古霉素治療，會因?yàn)橄魅跣∧c先天免疫力而增加有抵抗力的細(xì)菌所造成的感染,。
在接受該抗生素的小鼠中,，抗菌蛋白RegIIIγ在小腸的表達(dá)被抑制。RegIIIγ對于治療對萬古霉素有抵抗力的細(xì)菌腸球菌（Enterococcus (VRE)）所造成的感染療效顯著,，該細(xì)菌是造成住院患者感染的一個常見原因,。因此，能夠提高這種蛋白水平的療法（如口服脂多糖）也許可用于接受廣譜抗生素治療的患者,。（生物谷Bioon.com）
生物谷推薦原始出處：
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.
