| کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن | 
|---|---|---|---|---|
| 8501434 | 1553841 | 2018 | 7 صفحه PDF | دانلود رایگان | 
عنوان انگلیسی مقاله ISI
												Imidazole decreases the ampicillin resistance of an Escherichia coli strain isolated from a cow with mastitis by inhibiting the function of autoinducer 2
												
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																																												کلمات کلیدی
												
											موضوعات مرتبط
												
													علوم زیستی و بیوفناوری
													علوم کشاورزی و بیولوژیک
													علوم دامی و جانورشناسی
												
											پیش نمایش صفحه اول مقاله
												 
												چکیده انگلیسی
												Extended-spectrum β-lactamase-positive Escherichia coli is an important causative agent of mastitis in dairy cows that results in reduced milk production and quality, and is responsible for severe economic losses in the dairy industry worldwide. The quorum sensing signaling molecule autoinducer 2 (AI-2) is produced by many species of gram-negative and gram-positive bacteria, and might be a universal language for intraspecies and interspecies communication. Our previous work confirmed that exogenous AI-2 increases the antibiotic resistance of extended-spectrum β-lactamase-positive E. coli to the β-lactam group of antibiotics by upregulating the expression of the TEM-type β-lactamase. In addition, this regulation relies on the function of the intracellular AI-2 receptor LsrR. In the present work, we reported that exogenous imidazole, a furan carbocyclic analog of AI-2, decreases the antibiotic resistance of a clinical E. coli strain to β-lactam antibiotics by inhibiting the function of AI-2.
											ناشر
												Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Journal of Dairy Science - Volume 101, Issue 4, April 2018, Pages 3356-3362
											Journal: Journal of Dairy Science - Volume 101, Issue 4, April 2018, Pages 3356-3362
نویسندگان
												Lumin Yu, Wenchang Li, Ming Zhang, Yunmei Cui, Xiaolin Chen, Jingtian Ni, Li Yu, Fei Shang, Ting Xue,