RegIIIβ promotes Salmonella Typhimurium colonization of the gut in the early-stage gastrointestinal infection by enhancing flagella-driven locomotion

The bactericidal lectin RegIIIβ secreted by intestinal epithelial cells, kills the microbiota and enteropathogens but also been suggested to modulate bacterial physiology and host interactions. However, it remains to be determined whether RegIIIβ plays roles beyond its bactericidal effects. The present study revealed that RegIIIβ binds to the enteropathogen Salmonella enterica serovar Typhimurium in the gut, thereby increasing the locomotion speed of this bacterium through maintenance of the membrane potential. This led to enhanced invasion by S. Typhimurium into epithelial cells. Finally, RegIIIβ facilitated the gut colonization levels of S. Typhimurium and enteropathy in the early stages of gastrointestinal infection. In conclusion, S. Typhimurium has become tolerant to RegIIIβ in the evolutionary process, in which the pathogen has simultaneously become able to exploit this antimicrobial to enhance flagellar-based locomotion speed for successful gastrointestinal infection. Our findings provide novel insight into the roles of RegIIIβ in gastrointestinal infection caused by S. Typhimurium.由肠上皮细胞分泌的杀菌凝集素（bactericidal lectin）RegIIIβ，可杀灭肠道微生物群与肠道致病菌，同时被认为可调控细菌生理过程及宿主互作。然而，RegIIIβ是否具备杀菌效应之外的功能，仍有待明确。本研究揭示，RegIIIβ可与肠道内的鼠伤寒沙门氏菌（Salmonella enterica serovar Typhimurium）结合，通过维持其膜电位提升该菌的运动速度，进而增强该菌对上皮细胞的侵袭能力。最终，RegIIIβ可在胃肠道感染早期促进鼠伤寒沙门氏菌的肠道定植水平与肠道致病效应。综上，在进化历程中，鼠伤寒沙门氏菌已对RegIIIβ产生耐受性，且该病原体同时获得了利用这一抗菌物质提升鞭毛驱动运动速度的能力，以实现成功的胃肠道感染。本研究结果为理解RegIIIβ在鼠伤寒沙门氏菌引发的胃肠道感染中的作用提供了全新视角。