Atypical enteropathogenic Escherichia coli (aEPEC) is an important etiological agent of infantile diarrhea worldwide, including Brazil. The central mechanism of aEPEC pathogenesis is the ability to cause attaching-effacing lesions on intestinal epithelium, a property triggered by proteins encoded on a pathogenicity island called locus of enterocyte effacement. However, some strains produce an important non-LEE-encoded effector protein named EspFu, which is involved in the formation of A/E lesions and colonization of the intestinal epithelium, and thus may contribute to the pathogenicity of aEPEC. According to this, a study recently conducted in our laboratory demonstrated the participation of EspFu on LEE gene expression and adhesion of a nonadherent aEPEC isolate, suggesting a possible new role played by this protein. The espFu gene is commonly detected among pathogenic aEPEC O55:H7 strains, indicating that this protein may play an important role on pathogenesis of this group. Thus, the main objective of this work is to investigate the role of EspFu protein on aEPEC pathogenesis, using an espFu-positive O55:H7 strain as study model. Therefore, it will be examined the temporal expression and production of EspFu in aEPEC O55:H7 during the infection of intestinal epithelial cells. Further, an aEPEC espFu mutant will be compared to wild type and espFu-complemented mutant strains with respect to motility, biofilm formation, expression of the LEE operons, interaction with cultured epithelial cells and intestinal colonization of streptomycin-treated mice. Thus, we intend to better understand the contribution of EspFu to aEPEC pathogenesis, as well as to describe a new role played by this protein on bacterial cell compartment.
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