['With the increasing problem of resistance in pathogenic microorganisms the development of nonantimicrobial therapies is important. Diabetes mellitus (DM) is associated with an increased incidence of urinary tract infections. The majority of Escherichia coli strains, which is the most prevalent uropathogen, have type 1 fimbriae that bind to uroplakin in the bladder, as mediated by the adhesin FimH. A vaccine is being developed based on FimH adhesion.', 'The sequence of FimH adhesion of 29 E. coli strains isolated from women with DM was determined. For adherence experiments we used E. coli isolated from women with DM and a T24 bladder cell line as well as the 2 well-defined type 1 fimbriated E. coli strains Ctrl 39 and NU14, and uroepithelial cells from women with DM.', 'The fimH sequence of E. coli strains isolated from women with DM was highly homologous to the known fimH sequence of E. coli from patients without DM. Adherence assays in a T24 bladder cell line showed that adherence of these E. coli strains from women with DM could be inhibited by pre-incubation with antiserum raised against the chaperone-adhesin complex FimC-FimH. AntiFimCH antiserum also inhibited the adherence of the 2 well-defined E. coli strains expressing type 1 fimbriae, NU14 and Ctrl 39, but not of the FimH mutant strain NU14 H-, to uroepithelial cells from women with DM.'] Does fimch antiserum inhibit the adherence of Escherichia coli to cells collected by voided urine specimens of diabetic women?