Summary of project PR002696
This data is available at the NIH Common Fund's National Metabolomics Data Repository (NMDR) website, the Metabolomics Workbench, https://www.metabolomicsworkbench.org, where it has been assigned Project ID PR002696. The data can be accessed directly via it's Project DOI: 10.21228/M85K1P This work is supported by NIH grant, U2C- DK119886.
See: https://www.metabolomicsworkbench.org/about/howtocite.php
| Project ID: | PR002696 |
| Project DOI: | doi: 10.21228/M85K1P |
| Project Title: | Amino Acid Decarboxylation Preserves Salmonella Fitness During Phagocyte-Derived Oxidative Stress |
| Project Summary: | Successful establishment of infection by non-typhoidal Salmonella depends upon its ability to resist the antimicrobial defenses of the host innate immune response. To withstand the membrane depolarization that potentiates the killing activity of reactive oxygen species (ROS) produced by the phagocyte NADPH oxidase, Salmonella employs metabolic adaptations that maintain intracellular pH homeostasis and membrane energetics. Here, we identify amino acid decarboxylation as a critical determinant of Salmonella virulence and resistance to the oxidative pressures within the host environment. The proton-consuming decarboxylation of L-arginine preserves intracellular ∆pH and enhances Salmonella survival against the bactericidal effects of ROS, while downstream polyamine biosynthesis aids in bacterial recovery following ROS exposure. Polyamines alone cannot substitute for the immediate, protective impact of proton 26 consuming decarboxylation during oxidative stress killing. Specifically, we show that Salmonella relies on the combined activity of the inducible arginine AdiA and ornithine SpeF decarboxylases for resistance to oxidative stress, and that this activity is essential for Salmonella virulence during systemic infection. Together, amino acid decarboxylation and polyamine biosynthesis play complementary, but distinct roles in Salmonella adaptation to phagocyte-derived oxidative stress, providing a new framework for understanding how amino acid catabolism influences bacterial survival in the host |
| Institute: | University of Colorado School of Medicine |
| Department: | Immunology and Microbiology |
| Last Name: | Stephenson |
| First Name: | Daniel |
| Address: | Research 1 South L18-1303 12801 E. 17th Ave., Aurora, Colorado, 80045, USA |
| Email: | daniel.stephenson@cuanschutz.edu |
| Phone: | 303-724-3339 |
Summary of all studies in project PR002696
| Study ID | Study Title | Species | Institute | Analysis(* : Contains Untargted data) | Release Date | Version | Samples | Download(* : Contains raw data) |
|---|---|---|---|---|---|---|---|---|
| ST004270 | Amino Acid Decarboxylation Preserves Salmonella Fitness During Phagocyte-Derived Oxidative Stress | Salmonella enterica | University of Colorado School of Medicine | MS | 2025-10-31 | 1 | 10 | Uploaded data (3.9G)* |
