title: Escherichia coli F-18 phase locked 'on' for expression of type 1 fimbriae is a poor colonizer of the streptomycin-treated mouse large intestine.
abstract: Escherichia coli F-18, a human fecal isolate, makes type 1 fimbriae in vitro and in the streptomycin-treated mouse large intestine in vivo, and is an excellent colonizer of the cecal mucus layer in the streptomycin-treated mouse large intestine. E. coli F-18(pPKL91) harbors an extra fimB gene on a parB stabilized pPBR322 plasmid and is therefore phase-locked 'on' such that all cells express type 1 fimbriae. E. coli F-18(pPR633) contains essentially the same plasmid minus the fimB gene and in L-broth about 30% of the cells express type 1 fimbriae. When fed alone to streptomycin-treated mice, E. coli F-18(pPKL91) colonized the large intestine at about 10(7) cfu/g of feces. However, when simultaneously fed with E. coli F-18(pPR633) at either high (10(10) cfu), or low doses (10(4) cfu), E. coli F-18(pPKL91) was a poor colonizer dropping to a level of between 10(2) and 10(3) cfu/g of feces. When given enough time to establish the state of colonization (10 days), E. coli F-18(pPKL91) persisted in feces in high numbers despite subsequent challenge by E. coli F-18(pPR633). Moreover, although both E. coli F-18(pPR633) and E. coli F-18(pPKL91) grew equally well in cecal mucus in vitro, E. coli F-18(pPR633) traveled through a layer of cecal mucus in vitro much faster than E. coli F-18(pPKL91). Together, the data suggest that type 1 fimbriated cells are at a disadvantage in initiating the colonization state because they have difficulty entering the mucus layer of the intestine as rapidly as non-fimbriated cells. The data also point to the possible biological significance of type 1 fimbrial phase-variation in the mouse large intestine.
authors.affiliation: Department of Microbiology, University of Rhode Island, Kingston 02881.
authors.forename: B A
authors.initials: BA
authors.lastname: McCormick
authors.forename: P
authors.initials: P
authors.lastname: Klemm
authors.forename: K A
authors.initials: KA
authors.lastname: Krogfelt
authors.forename: R L
authors.initials: RL
authors.lastname: Burghoff
authors.forename: L
authors.initials: L
authors.lastname: Pallesen
authors.forename: D C
authors.initials: DC
authors.lastname: Laux
authors.forename: P S
authors.initials: PS
authors.lastname: Cohen
mesh_terms: D000818:Animals; D001422:Bacterial Adhesion; D001426:Bacterial Proteins / Q000096:biosynthesis* / Q000235:genetics / Q000378:metabolism*; D002432:Cecum / Q000382:microbiology*; D007446:Chromosome Inversion; D004268:DNA-Binding Proteins / Q000235:genetics / Q000378:metabolism* / Q000502:physiology*; D004926:Escherichia coli / Q000235:genetics / Q000472:pathogenicity / Q000502:physiology*; D029968:Escherichia coli Proteins; D036781:Fimbriae Proteins; D010861:Fimbriae, Bacterial / Q000502:physiology*; D015964:Gene Expression Regulation, Bacterial; D005812:Genes, Switch; D019426:Integrases; D007413:Intestinal Mucosa / Q000382:microbiology; D051379:Mice; D009876:Operon; D010957:Plasmids; D013307:Streptomycin / Q000494:pharmacology
chemical_list: D001426:Bacterial Proteins; D004268:DNA-Binding Proteins; D029968:Escherichia coli Proteins; C081956:fimB protein, E coli; C081955:fimE protein, E coli; C063055:fimbrillin; D036781:Fimbriae Proteins; D019426:Integrases; D013307:Streptomycin