C-di-AMP signaling in S. aureus

NIH RePORTER · NIH · R01 · $587,828 · view on reporter.nih.gov ↗

Abstract

Abstract Staphylococcus aureus is a leading cause of human morbidity and mortality, causing infection of the skin and soft tissues, post-surgical wounds, and lung infection among influenza and cystic fibrosis patients. Widespread multi-drug resistance has made eradication of S. aureus increasingly challenging, necessitating a deeper understanding of the physiology and pathogenesis associated with these organisms. A key aspect of bacterial survival and adaptation to altered environmental conditions is the ability to rapidly alter cellular behavior through second messenger signal transduction. C-di-AMP has recently emerged as a key regulator of bacterial physiology, pathogenesis, and immune activation. In the context of S. aureus, we believe that c- di-AMP produced by S. aureus has three important roles; (i) as a signaling molecule that mediates S. aureus metabolism and antibiotic resistance, (ii) as a bacterial PAMP that promotes pathological inflammation and host susceptibility to bacterial infection, and (iii) as a mediator of inter-bacterial signaling that alters the outcome of co-infections. Findings from these studies may have significant impacts on the course of antibiotic therapy during S. aureus infection and may uncover a novel target to eradicate recalcitrant S. aureus and the inflammation itpromotes.

Key facts

NIH application ID
9858253
Project number
5R01AI139071-02
Recipient
UNIVERSITY OF WASHINGTON
Principal Investigator
Joshua Woodward
Activity code
R01
Funding institute
NIH
Fiscal year
2020
Award amount
$587,828
Award type
5
Project period
2019-02-01 → 2024-01-31