Son Dae-Hyun, Kim Eun-Jung, Matin Abdul, Jung Suk-Yul
Department of Biomedical Laboratory Science, Molecular Diagnostics Research Institute, Namseoul University, 91 Daehak-ro, Seonghwan-eup, Cheonan, 31020, Republic of Korea.
Department of Biomedical Laboratory Science, Sangji University, Wonju, 220-702, Republic of Korea.
Parasitol Res. 2022 Jun;121(6):1805-1809. doi: 10.1007/s00436-022-07513-8. Epub 2022 Apr 11.
Naegleria fowleri can cause acute primary amoebic encephalitis. It is known that contact-dependent pathogenicity in free-living amoeba may be mediated through a carbohydrate-dependent pathway. In this study, the effect of mannose on the interaction between N. fowleri and pathogenic Escherichia coli O157:H7 and non-pathogenic E. coli DH5α was analyzed. In particular, the changes in proteases expressed by N. fowleri in response to mannose were analyzed. Unlike the conventional method, mannose was treated with N. fowleri for 1 h. The association between N. fowleri and E. coli O157:H7 treated with 50-mM and 100-mM mannose was significantly reduced by approximately 70.9% and 128.5%, respectively. E. coli O157:H7 invasion was reduced by about 10.8% by 100-mM mannose. Moreover, as a result of culturing N. fowleri invaded by E. coli O157:H7 for 24 h, E. coli O157:H7 also grew about 1.2 times in the group not treated with mannose. E. coli DH5α association was reduced by 25.7% by 100-mM mannose. On the other hand, there was almost no inhibitory effect by 100-mM glucose. In the analysis in which mannose bound to either N. fowleri or bacteria and affected the interaction, there was little effect on the interaction between N. fowleri and bacteria. In zymographic analysis, about 135-kDa and 75-kDa bands were observed by 50-mM and 100-mM mannose, and two bands were significantly increased by 100-mM mannose. This study suggests that mannose can be mediated in the contact-dependent pathway of N. fowleri and will serve as a basis for inducing changes in the protease of N. fowleri by other monosaccharides.
福氏耐格里阿米巴可引起急性原发性阿米巴脑炎。已知自由生活阿米巴的接触依赖性致病性可能通过碳水化合物依赖性途径介导。在本研究中,分析了甘露糖对福氏耐格里阿米巴与致病性大肠杆菌O157:H7和非致病性大肠杆菌DH5α之间相互作用的影响。特别地,分析了福氏耐格里阿米巴响应甘露糖而表达的蛋白酶的变化。与传统方法不同,甘露糖与福氏耐格里阿米巴处理1小时。用50 mM和100 mM甘露糖处理后,福氏耐格里阿米巴与大肠杆菌O157:H7之间的结合分别显著降低了约70.9%和128.5%。100 mM甘露糖使大肠杆菌O157:H7的侵袭减少了约10.8%。此外,将被大肠杆菌O157:H7侵袭的福氏耐格里阿米巴培养24小时后,在未用甘露糖处理的组中,大肠杆菌O157:H7也生长了约1.2倍。100 mM甘露糖使大肠杆菌DH5α的结合减少了25.7%。另一方面,100 mM葡萄糖几乎没有抑制作用。在甘露糖与福氏耐格里阿米巴或细菌结合并影响相互作用的分析中,对福氏耐格里阿米巴与细菌之间的相互作用几乎没有影响。在酶谱分析中,50 mM和100 mM甘露糖观察到约135 kDa和75 kDa的条带,100 mM甘露糖使两条带显著增加。本研究表明,甘露糖可在福氏耐格里阿米巴的接触依赖性途径中起介导作用,并将作为其他单糖诱导福氏耐格里阿米巴蛋白酶变化的基础。