Salmonella Typhoid Toxin PltB Subunit and Its Non-typhoidal Salmonella Ortholog Confer Differential Host Adaptation and Virulence.

摘要: Typhoidal and non-typhoidal Salmonelleae (NTS) cause typhoid fever gastroenteritis, respectively, in humans. Salmonella toxin contributes to disease progression chronic infection, but little is known about the role of its NTS ortholog. We found that ortholog induce different clinical presentations. The PltB subunit each exhibits glycan-binding preferences correlate with glycan expression profiles host cells targeted by bacterium at primary infection or intoxication sites. Through co-crystal structures subunits bound specific receptor moieties, we show they markedly virulence outcomes. Furthermore, immunization S. Javiana offers cross-reactive protection against lethal-dose challenge. Cumulatively, these results offer insights into evolution adaptations AB toxins, their cell tissue tropisms, design for improved vaccines therapeutics.