Mucosal Immunology and Biology Research Center, Division of Pediatric Gastroenterology and Nutrition, Massachusetts General Hospital, USA.
Department of Pediatrics, Harvard Medical School, Boston, MA, USA.
Gut Microbes. 2024 Jan-Dec;16(1):2331985. doi: 10.1080/19490976.2024.2331985. Epub 2024 Mar 28.
causes severe diarrheal disease worldwide. While many aspects of pathogenesis have been elucidated, significant knowledge gaps remain regarding the role of putative chromosomally-encoded virulence genes. The uncharacterized gene encoded on the chromosome has significant nucleotide sequence identity to the fluffy () antigen 43 autotransporter gene in pathogenic . Here, we constructed a Δ mutant in strain 2457T and examined the effects of this mutation on bacterial cell aggregation, biofilm formation, and adherence to colonic epithelial cells. Analyses included the use of growth media supplemented with glucose and bile salts to replicate small intestinal signals encountered by . Deletion of the gene in 2457T affected epithelial cell adherence, resulted in quicker bacterial cell aggregation, but did not affect biofilm formation. This work highlights a functional role for the gene in pathogenesis and further demonstrates the importance of using relevant and appropriate gastrointestinal signals to characterize virulence genes of enteropathogenic bacteria.
引起全球范围内严重的腹泻病。虽然发病机制的许多方面已经阐明,但关于假定染色体编码毒力基因的作用仍存在重大知识空白。染色体上未被阐明的基因与致病性 中的绒毛()抗原 43 自转运体基因具有显著的核苷酸序列同一性。在这里,我们构建了 2457T 菌株中的 Δ突变体,并研究了这种突变对细菌细胞聚集、生物膜形成和黏附结肠上皮细胞的影响。分析包括使用补充葡萄糖和胆汁盐的生长培养基来复制 遇到的小肠信号。2457T 中 基因的缺失影响上皮细胞黏附,导致细菌细胞更快聚集,但不影响生物膜形成。这项工作强调了 基因在 发病机制中的功能作用,并进一步证明了使用相关和适当的胃肠道信号来表征肠致病性细菌毒力基因的重要性。