Sialic Acid and N-Acetylglucosamine Regulate Type 1 Fimbriae Synthesis

Type 1 fimbriae of Escherichia coli, a member of the chaperon‐usher family of bacterial adhesins, are synthesised by the majority of strains of the bacterium. Although frequently produced by commensal strains, the adhesin is nevertheless a virulence factor in extraintestinal pathogenic E. coli (ExPEC). The role of the adhesin in pathogenesis is best understood in uropathogenic E. coli (UPEC). Host attachment and particularly invasion by type 1 fimbriate bacteria activates inflammatory pathways, with TLR4 signalling playing a predominant role (1). In a mouse model of cystitis, type 1 fimbriation not only enhances UPEC adherence to oligomannosides of uroplakin 1a on the surface of superficial umbrella cells of the bladder urothelium, but is both necessary and sufficient for their invasion (2, 3). Moreover, more surprisingly, the adhesin plays a role in the formation of transient intracellular bacterial communities (IBCs) within the cytoplasm of urothelial cells as part of UPEC cycles of invasion (4).