日前發(fā)表在英國《自然》（Nature）周刊上的一篇文章指出，使用抗生素有可能破壞腸道的先天免疫力,，這也是引起耐抗生素細菌感染的原因,。
研究人員對耐抗生素細菌感染原因進行了研究，這是一種廣泛使用抗生素導致的并發(fā)癥,，將使住院治療患者的身體健康受到更大的傷害,。
研究發(fā)現(xiàn)，盡管抗生素能夠消滅腸道中的很多細菌,，但由抗生素治療引起的腸道先天免疫功能的損傷也為耐抗生素細菌的繁殖提供了溫床,。
研究人員在觀察實驗鼠接受抗生素治療后的反應時，在其體內(nèi)發(fā)現(xiàn)了少量能夠抵抗微生物的腸蛋白RegⅢ伽馬,。這種腸蛋白能夠消滅耐萬古霉素腸球菌等高耐抗生素性細菌,。
據(jù)此,，科學家主張研發(fā)能夠提高腸內(nèi)RegⅢ伽馬蛋白含量的療法，以避免因使用抗生素而導致的細菌感染,。（生物谷Bioon.com）
生物谷推薦原始出處：
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
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-resistant Enterococcus (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 RegIII (also known as Reg3g), a secreted C-type lectin that kills Gram-positive bacteria, including VRE. Downregulation of RegIII 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 RegIII, 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.
