Type 1 fimbriae impair Antigen 43-mediated autoaggregation and may promote biofilm formation in Escherichia coli BW25113

Abstract

Biofilm formation is a key contributor to persistence, recurrence, and antibiotic resistance in uropathogenic Escherichia coli urinary tract infections. Two adhesins that play a role in the biofilm life cycle are Antigen 43 (encoded by the flu gene), a self-associating autotransporter that promotes autoaggregation, and type 1 fimbriae (encoded by the fim genes), which mediate attachment to surfaces. Previous research has shown that the presence of type 1 fimbriae may decrease Antigen 43-mediated autoaggregation, but their interactions and the necessity of Antigen 43 for autoaggregation remain unclear. Using E. coli BW25113 strains deficient in ∆flu or ∆fimD, we expressed Antigen 43 using an inducible plasmid and assessed growth, autoaggregation, and biofilm formation. Induced Antigen 43 expression transiently impaired growth and resulted in significant autoaggregation compared to non-Antigen 43 expressing strains. Concurrent repression of type 1 fimbriae expression in Antigen 43-expressing ∆flu strains increased autoaggregation to levels similar to fimD deficient strains expressing Antigen 43. Finally, type 1 fimbriae repression impaired biofilm formation in the absence of Antigen 43 expression. These findings provide new insight into the early stages of the E. coli biofilm life cycle, which may help clarify the pathogenesis of urinary tract infections and highlight potential targets for therapeutic strategies, particularly in the context of antibiotic-resistant uropathogenic E. coli.