Fibrinolytic-deficiencies predispose hosts to septicemia from a catheter-associated UTI

Jonathan J. Molina, Kurt N. Kohler, Christopher Gager, Marissa J. Andersen, Ellsa Wongso, Elizabeth R. Lucas, Andrew Paik, Wei Xu, Deborah L. Donahue, Karla Bergeron, Aleksandra Klim, Michael G. Caparon, Scott J. Hultgren, Alana Desai, Victoria A. Ploplis, Matthew J. Flick, Francis J. Castellino and Ana L. Flores-Mireles ()
Additional contact information
Jonathan J. Molina: University of Notre Dame
Kurt N. Kohler: University of Notre Dame
Christopher Gager: University of Notre Dame
Marissa J. Andersen: University of Notre Dame
Ellsa Wongso: University of Notre Dame
Elizabeth R. Lucas: University of Notre Dame
Andrew Paik: University of Notre Dame
Wei Xu: Washington University School of Medicine
Deborah L. Donahue: University of Notre Dame
Karla Bergeron: Washington University School of Medicine
Aleksandra Klim: Washington University School of Medicine
Michael G. Caparon: Washington University School of Medicine
Scott J. Hultgren: Washington University School of Medicine
Alana Desai: Washington University School of Medicine
Victoria A. Ploplis: University of Notre Dame
Matthew J. Flick: University of North Carolina
Francis J. Castellino: University of Notre Dame
Ana L. Flores-Mireles: University of Notre Dame

Nature Communications, 2024, vol. 15, issue 1, 1-16

Abstract: Abstract Catheter-associated urinary tract infections (CAUTIs) are amongst the most common nosocomial infections worldwide and are difficult to treat partly due to development of multidrug-resistance from CAUTI-related pathogens. Importantly, CAUTI often leads to secondary bloodstream infections and death. A major challenge is to predict when patients will develop CAUTIs and which populations are at-risk for bloodstream infections. Catheter-induced inflammation promotes fibrinogen (Fg) and fibrin accumulation in the bladder which are exploited as a biofilm formation platform by CAUTI pathogens. Using our established mouse model of CAUTI, here we identified that host populations exhibiting either genetic or acquired fibrinolytic-deficiencies, inducing fibrin deposition in the catheterized bladder, are predisposed to severe CAUTI and septicemia by diverse uropathogens in mono- and poly-microbial infections. Furthermore, here we found that Enterococcus faecalis, a prevalent CAUTI pathogen, uses the secreted protease, SprE, to induce fibrin accumulation and create a niche ideal for growth, biofilm formation, and persistence during CAUTI.

Date: 2024
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DOI: 10.1038/s41467-024-46974-6

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