Strain and host-cell dependent role of type-1 fimbriae in the adherence phenotype of super-shed Escherichia coli O157:H7

Authors

• Robab Katani, Huck Institutes of the Life Sciences
• Indira T. Kudva, USDA ARS National Animal Disease CenterFollow
• Sreenidhi Srinivasan, Huck Institutes of the Life Sciences
• Judith B. Stasko, USDA ARS National Animal Disease Center
• Megan Schilling, Huck Institutes of the Life Sciences
• Lingling Li, Pennsylvania State University
• Rebecca Cote, Huck Institutes of the Life Sciences
• Chitrita DebRoy, Pennsylvania State University
• Terrance M. Arthur, USDA ARS Roman L. Hruska U.S. Meat Animal Research Center
• Evgeni V. Sokurenko, University of Washington
• Vivek Kapur, USDA-ARSFollow

Date of this Version

5-1-2021

Document Type

Article

Citation

International Journal of Medical Microbiology 311 (2021) 151511

https://doi.org/10.1016/j.ijmm.2021.151511

Comments

This is an open access article under the CC BY-NC-ND license

Abstract

Super-shed (SS) Escherichia coli O157 (E. coli O157) demonstrate a strong, aggregative, locus of enterocyte effacement (LEE)-independent adherence phenotype on bovine recto-anal junction squamous epithelial (RSE) cells, and harbor polymorphisms in non-LEE-adherence-related loci, including in the type 1 fimbriae operon. To elucidate the role of type 1 fimbriae in strain- and host-specific adherence, we evaluated the entire Fim operon (FimB-H) and its adhesion (FimH) deletion mutants in four E. coli O157 strains, SS17, SS52, SS77 and EDL933, and evaluated the adherence phenotype in bovine RSE and human HEp-2 adherence assays. Consistent with the prevailing dogma that fimH expression is genetically switched off in E. coli O157, the ΔfimHSS52, ΔfimB-HSS52, ΔfimB-HSS17, and ΔfimHSS77 mutants remained unchanged in adherence phenotype to RSE cells. In contrast, the ΔfimHSS17 and ΔfimB-HSS77 mutants changed from a wild-type strong and aggregative, to a moderate and diffuse adherence phenotype, while both ΔfimHEDL933 and ΔfimB-HEDL933 mutants demonstrated enhanced binding to RSE cells (p < 0.05). Additionally, both ΔfimHSS17 and ΔfimHEDL933 were non-adherent to HEp-2 cells (p < 0.05). Complementation of the mutant strains with their respective wild-type genes restored parental phenotypes. Microscopy revealed that the SS17 and EDL933 strains indeed carry type 1 fimbriae-like structures shorter than those seen in uropathogenic E. coli. Taken together, these results provide compelling evidence for a strain and host cell type-dependent role of fimH and the fim operon in E. coli O157 adherence that needs to be further evaluated.