Host Cell Invasion and Urolithiasis Sample Clauses

Host Cell Invasion and Urolithiasis. P. mirabilis has been shown to invade a variety of cell lines, including monkey renal parenchymal cells, human bladder cell lines, human urothelium, and primary human renal cells (67, 69, 77-79). The swarmer cell morphotype is associated with the invasion of uroepithelial cells (77), and hyperswarming strains are more invasive than their wild- type counterparts (79). The expression of virulence factors such as zapA and hemolysin is coupled with differentiated swarmer cells likely aiding their increased invasiveness (64, 75). Invasion of host cells is hindered when flagella are immobilized, and flagellar mutants are less invasive than wild-type (69). Moreover, host cell invasion may provide protection against antibiotics for internalized P. mirabilis (80). The formation of urinary stones (urolithiasis) requires the production of urease for the precipitation of calcium and magnesium which results in the formation of crystals (67). P. mirabilis has been visualized within urinary stones (81), an environment that could promote persistence by protecting the bacteria from the immune response. Metabolic changes due to nutrient limiting conditions within the urinary stone may help the bacteria resist antibiotics (68). Recently, it was shown urolithiasis is dependent on MR/P fimbria which promotes aggregation of P. mirabilis in the urinary tract. These aggregates form urease-mediated crystals causing an influx of neutrophils which release neutrophil extracellular traps (NETs). NET formation in the urinary tract has been shown to be specific to P. mirabilis-mediated infection (82), and NETs could provide material to mediate further aggregation of cells and contribute to urolithiasis (83).
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