title: Type 1 pili are not necessary for colonization of the streptomycin-treated mouse large intestine by type 1-piliated Escherichia coli F-18 and E. coli K-12.
abstract: Escherichia coli F-18, an excellent colonizer of the streptomycin-treated mouse large intestine, produces type 1 pili. E. coli F-18 FimA-, type 1 pilus negative, and E. coli F-18 FimH-, type 1 pilus positive but adhesin negative, were constructed by bacteriophage P1 transduction of defective fimA and fimH genes from the E. coli K-12 strains ORN151 and ORN133, respectively, into E. coli F-18. Adhesion of E. coli F-18 to an immobilized mannose-bovine serum albumin glycoconjugate was about sixfold greater than that of either E. coli F-18 FimA- or E. coli F-18 FimH-, and adhesion of E. coli F-18 to immobilized cecal epithelial cell brush border membranes was between two- and threefold greater than that of E. coli F-18 FimA- or E. coli F-18 FimH-. When either E. coli F-18 FimA- or E. coli FimH- was fed to streptomycin-treated mice together with E. coli F-18, the pilus-negative and adhesin-negative strains colonized as well as their type 1-piliated parent. Essentially the same result was observed when the type 1-piliated E. coli K-12 strain ORN152 was fed to streptomycin-treated mice together with a nearly isogenic K-12 FimA- strain, ORN151. Furthermore, when streptomycin-treated mice were fed E. coli F-18 FimA- or E. coli F-18 FimH- together with E. coli F-18 Col-, which also makes type 1 pili but is a poor colonizer relative to E. coli F-18 because it grows poorly in mucus in the presence of E. coli F-18, the F-18 FimA- and F-18 FimH- strains colonized well (10(6) to 10(7) CFU/g of feces), whereas the number of E. coli F-18 Col- in feces decreased rapidly to 10(2) CFU/g of feces. These data show that in streptomycin-treated mice, the inability to produce functional type 1 pili has no effect on the ability of E. coli F-18 and E. coli K-12 to colonize the large intestine.
authors.affiliation: Department of Microbiology, University of Rhode Island, Kingston 02881-0812.
authors.forename: B A
authors.initials: BA
authors.lastname: McCormick
authors.forename: D P
authors.initials: DP
authors.lastname: Franklin
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 / Q000187:drug effects; D002432:Cecum / Q000382:microbiology*; D004926:Escherichia coli / Q000254:growth & development* / Q000502:physiology / Q000648:ultrastructure; D005243:Feces / Q000382:microbiology; D010861:Fimbriae, Bacterial / Q000502:physiology*; D008297:Male; D008358:Mannose; D051379:Mice; D008871:Microvilli / Q000382:microbiology; D009093:Mucus / Q000382:microbiology; D012709:Serum Albumin; D012710:Serum Albumin, Bovine; D013307:Streptomycin / Q000494:pharmacology*; D013440:Sulfides
chemical_list: D012709:Serum Albumin; D013440:Sulfides; C023840:mannose-bovine serum albumin conjugate; D012710:Serum Albumin, Bovine; D008358:Mannose; D013307:Streptomycin