Mechanisms to Evade the Phagocyte Respiratory Burst Arose by Convergent Evolution in Typhoidal Salmonella Serovars

• Main Authors: Hirotaka Hiyoshi, Tamding Wangdi, Gabriel Lock, Cheng Saechao, Manuela Raffatellu, Brian A. Cobb, Andreas J. Bäumler
• Format: Article
• Language: English
• Published: Elsevier 2018-02-01
• Series: Cell Reports
• Subjects: typhoid fever; capsular polysaccharide; paratyphoid fever; lipopolysaccharide; respiratory burst; neutrophil
• Online Access: http://www.sciencedirect.com/science/article/pii/S2211124718300330

Summary: Typhoid fever caused by Salmonella enterica serovar (S.) Typhi differs in its clinical presentation from gastroenteritis caused by S. Typhimurium and other non-typhoidal Salmonella serovars. The different clinical presentations are attributed in part to the virulence-associated capsular polysaccharide (Vi antigen) of S. Typhi, which prevents phagocytes from triggering a respiratory burst by preventing antibody-mediated complement activation. Paradoxically, the Vi antigen is absent from S. Paratyphi A, which causes a disease that is indistinguishable from typhoid fever. Here, we show that evasion of the phagocyte respiratory burst by S. Paratyphi A required very long O antigen chains containing the O2 antigen to inhibit antibody binding. We conclude that the ability to avoid the phagocyte respiratory burst is a property distinguishing typhoidal from non-typhoidal Salmonella serovars that was acquired by S. Typhi and S. Paratyphi A independently through convergent evolution.