As a leading cause of healthcare-associated infections, catheter-associated urinary tract infections (CAUTIs) present a unique challenge due to the high prevalence of multidrug-resistant and polymicrobial pathogens. Distinct from uncomplicated UTIs, the insertion of a urinary catheter provokes tissue damage that triggers inflammation, plasma extravasation, and the deposition of host fibrinogen. This inflammatory response drives the robust recruitment of immune cells and plasma extravasation, leading to the accumulation of fibrinogen─a key coagulation protein─on the device and bladder epithelium. This fibrinogen-rich environment creates a unique niche for intricate host–pathogen interactions. Crucially, uropathogens exploit these deposits to establish persistent biofilms, while the protein scaffold simultaneously modulates host immunity. Understanding these mechanisms, particularly the role of fibrinogen-binding adhesins, is vital for developing targeted, antimicrobial-sparing therapeutics. In this perspective, we examine the strategies uropathogens employ to persist in the catheterized bladder, the corresponding host immune response, and emerging strategies to prevent CAUTI.
Kohler et al. (Tue,) studied this question.