Abstract
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. The clinical presentation of typhoid fever differs from gastroenteritis, which has been attributed to the Salmonella enterica serovar (S.) Typhi capsular polysaccharide. Paradoxically, S. Paratyphi A is not capsulated but causes typhoid-like disease. Hiyoshi et al. show that the very long O antigen of S. Paratyphi A functions as a capsule, an example of convergent evolution.
Original language | English (US) |
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Pages (from-to) | 1787-1797 |
Number of pages | 11 |
Journal | Cell Reports |
Volume | 22 |
Issue number | 7 |
DOIs | |
State | Published - Feb 13 2018 |
Keywords
- capsular polysaccharide
- complement
- lipopolysaccharide
- natural IgM
- neutrophil
- paratyphoid fever
- respiratory burst
- typhoid fever
ASJC Scopus subject areas
- Biochemistry, Genetics and Molecular Biology(all)