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Metabolic incorporation of azides onto Helicobacter pylori cell surfaces
Author(s) -
Richardson Elizabeth,
Burns Sarah,
Dube Danielle H.
Publication year - 2008
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.22.2_supplement.325
Subject(s) - helicobacter pylori , azide , chemistry , cell , substrate (aquarium) , metabolism , biochemistry , bacteria , combinatorial chemistry , microbiology and biotechnology , biology , organic chemistry , genetics , ecology
We present a novel strategy for eliminating Helicobacter pylori from the human gastrointestinal tract. Our two‐step strategy capitalizes on (1) differences in metabolism of H. pylori versus mammalian cells to selectively incorporate azides on H. pylori cell surfaces, and (2) Staudinger ligation to covalently delivery therapeutic compounds to azide‐covered cells. Here we set out to accomplish the first step. Previous reports reveal the azide‐containing sugar peracetylated N ‐azidoacetylglucosamine (Ac 4 GlcNAz) is metabolized by mammalian cells but virtually excluded from their cell surfaces. We hypothesized that H. pylori would utilize Ac 4 GlcNAz as a metabolic substrate and incorporate azides on their cell surfaces. To test this hypothesis, H. pylori were grown in liquid media supplemented with Ac 4 GlcNAz. The presence of cell surface azides was probed via Staudinger ligation. Western blotting reveals that azides are metabolically incorporated into H. pylori proteins, suggesting that Ac 4 GlcNAz is utilized as a substrate in H. pylori . Intriguingly, H. pylori treated with Ac 4 GlcNAz display stunted growth and reduced motility compared to their untreated counterparts. These data suggest that treatment of patients with azide‐containing sugars might be the first step in a therapeutic strategy to decrease H. pylori infection. This work was supported by a Camille and Henry Dreyfus Faculty Start‐up Award to D.D.