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Effect of colicins on diarrheic Escherichia coli

机译:大肠菌素对腹泻性大肠杆菌的作用

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Shirazi Z. Tahamtan Y., Effect of colicins on diarrheic Escherichia coli, Onl J Vet Res., 19 (10): 653-662, 2015. Colicinogenic E. coli (CEC) strains were tested on verotoxin serotypes O157:H7 (clone 1), five Non-O157:H7 (clone 2) and eight K99 (clone3) strains. DEC and test strains were inoculated onto Luria bertani (LB) broth (O/N). O/N culture of CEC strains was spotted onto LA and LA supplemented mitomycin C (LAM) dry plates previously lawn with DEC. Plates were incubated O/N at 37°C and inhibitory activity against DEC strains was defined as a clear zone around colicin-producing strains. PCR was used to isolate positive and negative virulence factors among DEC strains and colicin gene in CEC strains. Inhibition of DEC strains occurred for 33.3to 94.4% of clones with most and least inhibition related to Col IaIb, E-mix and Col M respectively. The presence of mitomycin C in the LAM medium increased inhibition of colicins and those not inhibited on LA. Sensitivity of DEC strains to colicins wasDEC clone 1 >2 >3 on LA and DEC clone 2 >1 >3 on LAM. Inhibition on LAM medium may have been induced by injury to DEC strains by mitomycin C sensitivity. Insensitivities to colicins on LA and LAM could be due to wild-type DEC strains, immunity genes, loss of genes coding for outer membrane protein receptors, inherent genetic differences in genes regulating production of colicins, host cell SOS system or unknown mechanisms.
机译:Shirazi Z.Tahamtan Y.,大肠菌素对腹泻性大肠杆菌的作用,Onl J Vet Res。,19(10):653-662,2015.对产肠毒素的大肠杆菌(CEC)菌株进行了O157:H7血清毒素血清型测试(克隆1),五个Non-O157:H7(克隆2)和八个K99(克隆3)菌株。将DEC和测试菌株接种到Luria bertani(LB)肉汤(O / N)上。将CEC菌株的O / N培养物点样到LA和之前用DEC草坪的LA补充的丝裂霉素C(LAM)干板。将板在37℃下以O / N温育,并且将针对DEC菌株的抑制活性定义为产生大肠杆菌的菌株周围的透明区。 PCR用于分离CEC菌株的DEC菌株和大肠菌素基因之间的阳性和阴性毒力因子。 DEC菌株的抑制作用发生在33.3%至94.4%的克隆中,其抑制作用的最大和最小分别与Col IaIb,E-mix和Col M有关。 LAM培养基中丝裂霉素C的存在会增加对大肠菌素的抑制作用,而对LA则没有抑制作用。 DEC菌株对大肠菌素的敏感性是LA上的DEC克隆1> 2> 3,而LAM上的DEC克隆2> 1> 3。 LAM培养基的抑制作用可能是丝裂霉素C敏感性对DEC菌株的伤害所致。 LA和LAM对大肠菌素不敏感的原因可能是由于野生型DEC菌株,免疫基因,编码外膜蛋白受体的基因缺失,调控大肠菌素产生的基因固有的遗传差异,宿主细胞SOS系统或未知机制。

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