English (United Kingdom)

https://curated-unify.zendy.io/wp-json/zendy-region/v1/featured_content/oa?rat=en

https://curated-unify.zendy.io/wp-json/zendy-region/v1/highlighted_journal/

Global: Zendy Plus annual

Presents the access of premium content as premium feature

Premium Content

Presents the keyphrase highlighting as premium feature

Keyphrase Highlighting

Presents the summarisation as premium feature

Summarisation

Insights

Presents the pdf analysis as premium feature

PDF Analysis

Presents the zaia usage as premium feature

ZAIA

Global: Zendy Tools annual

Global: Zendy Free Plan

Global: Zendy Tools monthly

Global: Zendy Plus monthly

Vi capsular polysaccharide is a major virulence determinant of the human typhoid- causing pathogen Salmonella typhi; it is absent in nontyphoidal Salmonella serovars. We show in this study that through its specific interaction with the membrane recognition complex containing the prohibitin family of molecules, Vi can inhibit the production of inflammatory cytokines from mononuclear phagocytes stimulated with Salmonella flagellin. Remarkably, Vi lost this anti-inflammatory capability and switched to a proinflammatory state when cell stimulations were performed in the presence of serum. The serum-transformed proinflammatory form of Vi induced secretion of cytokines from monocytes by specifically engaging TLR-2/TLR-1. The molecule responsible for bringing about this conversion of Vi from an anti-inflammatory to a proinflammatory form was serum-derived hemoglobin. Derivatives of Vi incapable of interacting with hemoglobin did not switch to a proinflammatory state in vitro or in vivo. These findings provide compelling evidence for a role of hemoglobin in transforming the anti-inflammatory S. typhi virulence polysaccharide into an immune activator.

Hemoglobin Transforms Anti-Inflammatory Salmonella typhi Virulence Polysaccharide into a TLR-2 Agonist