Sialic acid and N-acetylglucosamine Regulate type 1 Fimbriae Synthesis

• Published in: Microbiology spectrum 2015-06, Vol.3 (3)
• Main Author: Blomfield, Ian C
• Format: Article
• Language: English
• Subjects: Acetylglucosamine; Acetylglucosamine - genetics; Acetylglucosamine - metabolism; Adhesins, Escherichia coli - genetics; Adhesins, Escherichia coli - metabolism; Animals; Bacterial Adhesion; Bacterial Adhesion - physiology; Bacterial Outer Membrane Proteins - genetics; Cystitis - microbiology; Escherichia coli Proteins - genetics; Fimbriae Proteins - biosynthesis; Fimbriae Proteins - genetics; Fimbriae, Bacterial; Fimbriae, Bacterial - genetics; Fimbriae, Bacterial - metabolism; Gene Expression Regulation, Bacterial; Mice; N-Acetylneuraminic Acid; N-Acetylneuraminic Acid - genetics; N-Acetylneuraminic Acid - metabolism; Porins - genetics; Receptors, Immunologic - metabolism; Review Article; Toll-Like Receptor 4 - metabolism; Uropathogenic Escherichia coli; Uropathogenic Escherichia coli - genetics; Uropathogenic Escherichia coli - metabolism; Uropathogenic Escherichia coli - pathogenicity; Urothelium - microbiology; Virulence Factors - genetics; Virulence Factors - metabolism
• ISSN: 2165-0497; 2165-0497
• DOI: 10.1128/microbiolspec.MBP-0015-2014

Type 1 fimbriae of E. coli, a chaperon-usher bacterial adhesin, are synthesized 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 invasion by type 1 fimbriate bacteria activates inflammatory pathways, with TLR4 signaling playing a predominant role. In a mouse model of cystitis, type 1 fimbriation not only enhances UPEC adherence to the surface of superficial umbrella cells of the bladder urothelium, but is both necessary and sufficient for their invasion. Moreover 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. The expression of type 1 fimbriation is controlled by phase variation at the transcriptional level, a mode of gene regulation in which bacteria switch reversibly between fimbriate and afimbriate phases. Phase variation has been widely considered to be a mechanism enabling immune evasion. Notwithstanding the apparently random nature of phase variation, switching of type 1 fimbrial expression is nevertheless controlled by a range of environmental signals that include the amino sugars sialic acid and N-acetylglucosamine (GlcNAc). Sialic acid plays a pivotal role in innate immunity, including signaling by the toll-like receptors. Here how sialic acid and GlcNAc control type 1 fimbriation is described and the potential significance of this regulatory response is discussed.