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

Cell Rep. 2018 Feb 13;22(7):1787-1797. doi: 10.1016/j.celrep.2018.01.016.

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.

Keywords: capsular polysaccharide; complement; lipopolysaccharide; natural IgM; neutrophil; paratyphoid fever; respiratory burst; typhoid fever.

Publication types

  • Research Support, N.I.H., Extramural
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adult
  • Animals
  • Antibodies / metabolism
  • Antigens, Bacterial / metabolism
  • Biological Evolution*
  • Complement Activation
  • HL-60 Cells
  • Humans
  • Mice
  • Models, Biological
  • Neutrophils / metabolism
  • Phagocytes / microbiology*
  • Reactive Oxygen Species / metabolism
  • Respiratory Burst*
  • Salmonella typhi / physiology*
  • Serogroup*
  • Typhoid Fever / microbiology*
  • Typhoid Fever / pathology*

Substances

  • Antibodies
  • Antigens, Bacterial
  • Reactive Oxygen Species