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作 者:吴同垒[1] 冀梦瑶 周诗淼 张莹辉[2] 李佩国[1] 蒋卉[2] WU Tonglei;JI Mengyao;ZHOU Shimiao;ZHANG Yinghui;LI Peiguo;JIANG Hui(Key Laboratory of Preventive Veterinary Medicine of Hebei Province,Hebei Normal University of Science&Technology,Qinhuangdao,Hebei 066600,China;China Institute of Veterinary Drug Supervision,Beijing 100800,China)
机构地区:[1]河北科技师范学院河北省预防兽医学重点实验室,河北秦皇岛066004 [2]中国兽医药品监察所,北京100080
出 处:《中国兽医学报》2022年第5期920-925,共6页Chinese Journal of Veterinary Science
基 金:秦皇岛市科学技术研究与发展计划资助项目(201803B006);河北省现代农业产业体系技术体系蛋肉鸡产业创新团队资助项目(HBCT2018150206)。
摘 要:为研究肠炎沙门菌甘油激酶GlpK的功能,利用同源重组技术构建了肠炎沙门菌GlpK基因敲除株c50336ΔglpK,通过药物敏感性和生物被膜相关实验探究其在肠炎沙门菌生物被膜形成中的作用。研究结果显示,GlpK基因敲除后不影响细菌的体外生长,但可显著降低肠炎沙门菌形成生物被膜的能力和药物敏感性,且肠炎沙门菌Curli菌毛和纤维素的形成受到抑制,生物被膜相关基因的表达下调。研究结果表明GlpK基因参与肠炎沙门菌的耐药性和生物被膜形成,为肠炎沙门菌新型靶向药物的研发奠定了重要基础。To investigate the roles of GlpK of Salmonella enterica(S.enteritidis),the S.enteritidis GlpK knockout strain c50336ΔglpK was constructed by the homologous recombination technique.The role of GlpK in the biofilm formation of S.enteritidis was confirmed by drug sensitivity assay and biofilm related experiments.The results showed that the knockout strain c50336ΔglpK did not exhibit growth inhibition in vitro,but GlpK knockout significantly reduced the ability of S.enteritidis to form biofilm and drug sensitivity,and the formation of Curli pili and cellulose in S.enteritidis was inhibited,and the expression of biofilm-related genes was down-regulated.The results show that GlpK gene is involved in the drug resistance and biofilm formation of S.enteritidis,which laid an important foundation for the development of new targeted drugs.
分 类 号:S852.61[农业科学—基础兽医学] R535[农业科学—兽医学]
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