ArticlePLoS pathogens2025
Evasion of serum antibodies and complement by Salmonella Typhi and Paratyphi A.
Article in PLoS pathogens, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed.
- Protein-centric mechanisms of typhoidalFrontiers in cellular and infection microbiology · 2026Review
- Salmonella enterica persister cells exhibit distinct susceptibility profiles following exposure to human serum and macrophages.PloS one · 2026Article
- Associations Between Systemic Immunity Inflammation Index, Aggregate Index of Systemic Inflammation, and Hospital Acquired Otitis Media in Children Aged ≤12 years with Bacterial Pneumonia.Infection and drug resistance · 2026Article
- Integrative phenotypic and functional genomic characterization of virulence and antimicrobial resistance inFrontiers in microbiology · 2026Article
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Authors and funding
4 authors.
Funding
Abstract
Nontyphoidal and enteric fever serovars of Salmonella enterica display distinctive interactions with serum antibodies and the complement system, which initiate the host immune response to invading microbes. This study examines the contributions of lipopolysaccharide O-antigen (O-ag) and the S. Typhi Vi polysaccharide capsule to serum resistance, complement activation and deposition, and immunoglobulin (Ig) binding in nontyphoidal S. enterica serovar Typhimurium and the enteric fever serovars S. Typhi and S. Paratyphi A. Although all three serovars are resistant to serum killing, S. Typhi and S. Paratyphi A exhibit lower levels of Ig binding, complement binding and complement activation compared to S. Typhimurium. In S. Typhimurium, WzzB-dependent long O-antigen (L O-ag) production with 16-to-35 repeating O-ag units, and FepE-dependent very long O-antigen (VL O-ag) production with over 100 repeating O-ag units, are required for serum resistance but do not prevent IgM binding or complement deposition. S. Typhi lacks VL O-ag, but its production of Vi capsule inhibits IgM binding and complement deposition, while acting in concert with L O-ag to resist serum killing. In S. Paratyphi A, L O-ag production is deficient due to a hypofunctional WzzB protein, but this is compensated by greater quantities of VL O-ag, which are required for serum resistance. Restoration of WzzB function by exchange with the S. Typhimurium or S. Typhi wzzB alleles can restore L O-ag production in S. Paratyphi A but decreases VL O-ag production, resulting in increased IgM binding. Replacement of the S. Paratyphi A O2-type polysaccharide with the S. Typhi O9 polysaccharide further increases IgM binding of S. Paratyphi A, which enhances complement activation but not complement deposition. Lastly, a gene duplication of rfbV in S. Paratyphi A is necessary for higher levels of VL O-ag and resistance to complement deposition and antibody binding. Collectively, these observations demonstrate fundamental differences between nontyphoidal and enteric fever Salmonella serovars in their interactions with innate immune effectors. Whereas nontyphoidal S. Typhimurium elicits, exploits and withstands the host acute inflammatory response, the enteric fever serovars S. Typhi and S. Paratyphi A evade it by limiting antibody recognition and complement activation and deposition.
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