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Published on: May 6, 2018
Role of aggregate-forming pilus (AFP) in adherence and colonization of both intestinal and urinary tracts
Paulo A Schüroff1,2, Cecilia M Abe1, Jonatas W Silva1
1Laboratório de Bacteriologia, Instituto Butantan, São Paulo, Brazil.
Abstract:
Hybrid-pathogenic Escherichia coli represent an important group of strains associated with intestinal and extraintestinal infections. Recently, we described strain UPEC-46, a uropathogenic/enteroaggregative E. coli (UPEC/EAEC) strain presenting the aggregative adherence (AA) pattern on bladder and colorectal epithelial cells mediated by aggregate-forming pili (AFP). However, the role of AFP and other uninvestigated putative fimbriae operons in UPEC-46 pathogenesis remains unclear. Thus, this study evaluated the involvement of AFP and other adhesins in uropathogenicity and intestinal colonization using different in vitro and in vivo models. The strain UPEC-46 was able to adhere and invade intestinal and urinary cell lines. A library of transposon mutants also identified the involvement of type I fimbriae (TIF) in the adherence to HeLa cells, in addition to colorectal and bladder cell lines. The streptomycin-treated mouse in vivo model also showed an increased number of bacterial counts in the colon in the presence of AFP and TIF. In the mouse model of ascending urinary tract infection (UTI), AFP was more associated with kidney colonization, while TIF appears to mediate bladder colonization. Results observed in in vivo experiments were also confirmed by electron microscopy (EM) analyses. In summary, the in vitro and in vivo analyses show a synergistic role of AFP and TIF in the adherence and colonization of intestinal and urinary epithelia. Therefore, we propose that hybrid E. coli strains carrying AFP and TIF could potentially cause intestinal and urinary tract infections in the same patient.
Insights
Hybrid pathogenic Escherichia coli strains utilize aggregate-forming pili (AFP) and type I fimbriae (TIF) synergistically for intestinal and urinary tract colonization. These adhesins are crucial for infections in both systems.
Area of Science:
- Microbiology
- Infectious Diseases
- Bacterial Pathogenesis
Background:
- Hybrid-pathogenic *Escherichia coli* strains cause significant intestinal and extraintestinal infections.
- Aggregate-forming pili (AFP) mediate aggregative adherence in UPEC-46, a uropathogenic/enteroaggregative *E. coli* (UPEC/EAEC) strain.
- The precise roles of AFP and other fimbriae in UPEC-46 pathogenesis require elucidation.
Purpose of the Study:
- To investigate the involvement of AFP and other adhesins in the uropathogenicity and intestinal colonization of *E. coli* UPEC-46.
- To delineate the specific contributions of AFP and type I fimbriae (TIF) to adherence and invasion in relevant epithelial models.
- To assess the in vivo significance of these adhesins in both intestinal and urinary tract infection models.
Main Methods:
- In vitro adherence and invasion assays using intestinal and urinary epithelial cell lines.
- Construction and analysis of transposon mutants to identify key adhesins.
- In vivo studies utilizing streptomycin-treated mice for intestinal colonization and a murine ascending urinary tract infection model.
- Electron microscopy (EM) for visualizing bacterial adherence structures.
Main Results:
- UPEC-46 demonstrated adherence and invasion capabilities in both intestinal and urinary cell lines.
- Type I fimbriae (TIF) were identified as crucial for adherence to epithelial cells, alongside AFP.
- In vivo, both AFP and TIF enhanced bacterial counts in the colon, with AFP primarily associated with kidney colonization and TIF with bladder colonization.
Conclusions:
- Aggregate-forming pili (AFP) and type I fimbriae (TIF) play synergistic roles in the adherence and colonization of both intestinal and urinary epithelia.
- Hybrid *E. coli* strains possessing both AFP and TIF are likely to cause concurrent intestinal and urinary tract infections.
- Targeting these adhesins could offer novel therapeutic strategies against hybrid *E. coli* infections.
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