Journal
CELLULAR MICROBIOLOGY
Volume 9, Issue 9, Pages 2230-2241Publisher
WILEY
DOI: 10.1111/j.1462-5822.2007.00952.x
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Funding
- NICHD NIH HHS [K12HD00850] Funding Source: Medline
- NIDDK NIH HHS [P50DK64540, R01DK51406] Funding Source: Medline
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Uropathogenic Escherichia coli, the predominant causative agent of urinary tract infections, use type 1 pili to bind and invade bladder epithelial cells. Upon entry, the bacteria rapidly replicate and enter a complex developmental pathway ultimately forming intracellular bacterial communities (IBCs), a niche with biofilm-like properties protected from innate defences and antibiotics. Paradoxically, bacteria within IBCs produce type 1 pili, an organelle thought only to be an extracellular colonization factor. Thus, we investigated the function of type 1 pili in IBC development. The cystitis isolate, UTI89, was genetically manipulated for conditional fim expression under control of the tet promoter. In this strain, UTI89-tetR/P-tet fim, piliation is constitutively inhibited by the tetracycline repressor, TetR. Repression is relieved by anhydrotetracycline (AHT) treatment. UTI89-tetR/P-tet fim and the isogenic control strain, UTI89-tetR, grown in the presence of AHT, colonized the bladder and invaded the superficial umbrella cells at similar levels at early times in a murine model of infection. However, after invasion UTI89-tetR/P-tet fim became non-piliated and was unable to form typical IBCs comprised of tightly packed, coccoid-shaped bacteria in contrast to the control strain, UTI89-tetR. Thus, this work changes the extracellular colonization functional paradigm of pili by demonstrating their intracellular role in biofilm formation.
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