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

Cell Reports

Gabriel Lock¹  Manuela Raffatellu²  Cheng Saechao²  Tamding Wangdi²  Hirotaka Hiyoshi²  Andreas J. Bäumler³  Brian A. Cobb⁴ 

[1] Corresponding author;Department of Medical Microbiology and Immunology, School of Medicine, University of California, Davis, Davis, CA 95616, USA;Department of Pathology, School of Medicine, Case Western Reserve University, Cleveland, OH 44106, USA;Department of Pediatrics, School of Medicine, University of California San Diego, La Jolla, CA 92093, USA;

关键词: typhoid fever;    capsular polysaccharide;    paratyphoid fever;    lipopolysaccharide;    respiratory burst;    neutrophil;   

DOI  :  10.1016/j.celrep.2018.01.016

来源: DOAJ

【 摘 要 】

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.

【 授权许可】

Unknown