title: How type 1 fimbriae help Escherichia coli to evade extracellular antibiotics.
abstract: To survive antibiotics, bacteria use two different strategies: counteracting antibiotic effects by expression of resistance genes or evading their effects e.g. by persisting inside host cells. Since bacterial adhesins provide access to the shielded, intracellular niche and the adhesin type 1 fimbriae increases bacterial survival chances inside macrophages, we asked if fimbriae also influenced survival by antibiotic evasion. Combined gentamicin survival assays, flow cytometry, single cell microscopy and kinetic modeling of dose response curves showed that type 1 fimbriae increased the adhesion and internalization by macrophages. This was caused by strongly decreased off-rates and affected the number of intracellular bacteria but not the macrophage viability and morphology. Fimbriae thus promote antibiotic evasion which is particularly relevant in the context of chronic infections.
authors.affiliation: Laboratory of Applied Mechanobiology, Department of Health Sciences and Technology, ETH Zürich, 8093 Zürich, Switzerland.
authors.forename: Ima
authors.initials: I
authors.lastname: Avalos Vizcarra
authors.affiliation: Laboratory of Applied Mechanobiology, Department of Health Sciences and Technology, ETH Zürich, 8093 Zürich, Switzerland.
authors.forename: Vahid
authors.initials: V
authors.lastname: Hosseini
authors.affiliation: Laboratory of Applied Mechanobiology, Department of Health Sciences and Technology, ETH Zürich, 8093 Zürich, Switzerland.
authors.forename: Philip
authors.initials: P
authors.lastname: Kollmannsberger
authors.affiliation: Laboratory of Applied Mechanobiology, Department of Health Sciences and Technology, ETH Zürich, 8093 Zürich, Switzerland.
authors.forename: Stefanie
authors.initials: S
authors.lastname: Meier
authors.affiliation: Department of Biology, ETH Zürich, 8093 Zürich, Switzerland.
authors.forename: Stefan S
authors.initials: SS
authors.lastname: Weber
authors.affiliation: Department of Environmental Systems Science, ETH Zürich, 8092 Zürich, Switzerland.|Department of Environmental Microbiology, Eawag, 8600 Dübendorf, Switzerland.
authors.forename: Markus
authors.initials: M
authors.lastname: Arnoldini
authors.affiliation: Department of Environmental Systems Science, ETH Zürich, 8092 Zürich, Switzerland.|Department of Environmental Microbiology, Eawag, 8600 Dübendorf, Switzerland.
authors.forename: Martin
authors.initials: M
authors.lastname: Ackermann
authors.affiliation: Laboratory of Applied Mechanobiology, Department of Health Sciences and Technology, ETH Zürich, 8093 Zürich, Switzerland.
authors.forename: Viola
authors.initials: V
authors.lastname: Vogel
mesh_terms: D000818:Animals; D000900:Anti-Bacterial Agents / Q000494:pharmacology*; D001422:Bacterial Adhesion; D002460:Cell Line; D002470:Cell Survival; D024881:Drug Resistance, Bacterial; D004926:Escherichia coli / Q000187:drug effects* / Q000502:physiology*; D010861:Fimbriae, Bacterial; D015964:Gene Expression Regulation, Bacterial; D008247:Lysosomes / Q000276:immunology / Q000382:microbiology; D008264:Macrophages / Q000276:immunology / Q000378:metabolism / Q000382:microbiology; D051379:Mice; D050296:Microbial Viability / Q000187:drug effects / Q000276:immunology; D010587:Phagocytosis; D010641:Phenotype
chemical_list: D000900:Anti-Bacterial Agents