{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,5]],"date-time":"2026-10-05T13:51:20Z","timestamp":1791208280548,"version":"4.1.0"},"reference-count":52,"publisher":"American Society for Microbiology","issue":"3","license":[{"start":{"date-parts":[[2015,6,18]],"date-time":"2015-06-18T00:00:00Z","timestamp":1434585600000},"content-version":"tdm","delay-in-days":0,"URL":"https:\/\/journals.asm.org\/non-commercial-tdm-license"}],"content-domain":{"domain":["journals.asm.org"],"crossmark-restriction":true},"short-container-title":["Microbiol Spectr"],"published-print":{"date-parts":[[2015,6,18]]},"abstract":"<jats:title>ABSTRACT<\/jats:title>\n          <jats:p>\n            Type 1 fimbriae of\n            <jats:italic>E. coli<\/jats:italic>\n            , 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\n            <jats:italic>E. coli<\/jats:italic>\n            (ExPEC). The role of the adhesin in pathogenesis is best understood in Uropathogenic\n            <jats:italic>E. coli<\/jats:italic>\n            (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.\n          <\/jats:p>","DOI":"10.1128\/microbiolspec.mbp-0015-2014","type":"journal-article","created":{"date-parts":[[2015,6,26]],"date-time":"2015-06-26T12:01:30Z","timestamp":1435320090000},"update-policy":"https:\/\/doi.org\/10.1128\/asmj-crossmark-policy-page","source":"Crossref","is-referenced-by-count":9,"title":["Sialic acid and N-acetylglucosamine Regulate type 1 Fimbriae Synthesis"],"prefix":"10.1128","volume":"3","author":[{"given":"Ian C.","family":"Blomfield","sequence":"first","affiliation":[{"name":"School of Biosciences, University of Kent, Kent, UK"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"235","reference":[{"key":"e_1_3_1_2_2","doi-asserted-by":"crossref","unstructured":"Hannan TJ Totsika M Mansfield KJ Moore KH Schembri MA Hultgren SJ. 2012. 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