Yousuf Farzana Abubakar, Yousuf Zuhair, Iqbal Junaid, Siddiqui Ruqaiyyah, Khan Hafsa, Khan Naveed Ahmed
Department of Biological and Biomedical Sciences, Aga Khan University, Stadium Road, Karachi 74800, Pakistan.
Biomed Res Int. 2014;2014:265424. doi: 10.1155/2014/265424. Epub 2014 Apr 10.
Here we determined the role of various genomic islands in E. coli K1 interactions with phagocytic A. castellanii and nonphagocytic brain microvascular endothelial cells. The findings revealed that the genomic islands deletion mutants of RS218 related to toxins (peptide toxin, α -hemolysin), adhesins (P fimbriae, F17-like fimbriae, nonfimbrial adhesins, Hek, and hemagglutinin), protein secretion system (T1SS for hemolysin), invasins (IbeA, CNF1), metabolism (D-serine catabolism, dihydroxyacetone, glycerol, and glyoxylate metabolism) showed reduced interactions with both A. castellanii and brain microvascular endothelial cells. Interestingly, the deletion of RS218-derived genomic island 21 containing adhesins (P fimbriae, F17-like fimbriae, nonfimbrial adhesins, Hek, and hemagglutinin), protein secretion system (T1SS for hemolysin), invasins (CNF1), metabolism (D-serine catabolism) abolished E. coli K1-mediated HBMEC cytotoxicity in a CNF1-independent manner. Therefore, the characterization of these genomic islands should reveal mechanisms of evolutionary gain for E. coli K1 pathogenicity.
在此，我们确定了各种基因组岛在大肠杆菌K1与吞噬性卡氏棘阿米巴和非吞噬性脑微血管内皮细胞相互作用中的作用。研究结果表明，与毒素（肽毒素、α-溶血素）、黏附素（P菌毛、F17样菌毛、非菌毛黏附素、Hek和血凝素）、蛋白质分泌系统（溶血素的T1SS）、侵袭素（IbeA、CNF1）、代谢（D-丝氨酸分解代谢、二羟基丙酮、甘油和乙醛酸代谢）相关的RS218基因组岛缺失突变体与卡氏棘阿米巴和脑微血管内皮细胞的相互作用均减弱。有趣的是，缺失包含黏附素（P菌毛、F17样菌毛、非菌毛黏附素、Hek和血凝素）、蛋白质分泌系统（溶血素的T1SS）、侵袭素（CNF1）、代谢（D-丝氨酸分解代谢）的RS218衍生基因组岛21，以一种不依赖CNF1的方式消除了大肠杆菌K1介导的HBMEC细胞毒性。因此，对这些基因组岛的表征应能揭示大肠杆菌K1致病性进化获得的机制。
