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Molina, Jonathan J; Kohler, Kurt N; Gager, Christopher; Andersen, Marissa J; Wongso, Ellsa; Lucas, Elizabeth R; Paik, Andrew; Xu, Wei; Donahue, Deborah L; Bergeron, Karla; Klim, Aleksandra; Caparon, Michael G; Hultgren, Scott J; Desai, Alana; Ploplis, Victoria A; Flick, Matthew J; Castellino, Francis J; Flores-Mireles, Ana L
Nature communications, 03/2024, Letnik: 15, Številka: 1Journal Article
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.
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JCR | SNIP | JCR | SNIP | JCR | SNIP | JCR | SNIP |
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in: SICRIS
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