title: Lactobacilli Reduce Helicobacter pylori Attachment to Host Gastric Epithelial Cells by Inhibiting Adhesion Gene Expression.
abstract: The human gastrointestinal tract, including the harsh environment of the stomach, harbors a large variety of bacteria, of which Lactobacillus species are prominent members. The molecular mechanisms by which species of lactobacilli interfere with pathogen colonization are not fully characterized. In this study, we aimed to study the effect of lactobacillus strains upon the initial attachment of Helicobacter pylori to host cells. Here we report a novel mechanism by which lactobacilli inhibit adherence of the gastric pathogen H. pylori In a screen with Lactobacillus isolates, we found that only a few could reduce adherence of H. pylori to gastric epithelial cells. Decreased attachment was not due to competition for space or to lactobacillus-mediated killing of the pathogen. Instead, we show that lactobacilli act on H. pylori directly by an effector molecule that is released into the medium. This effector molecule acts on H. pylori by inhibiting expression of the adhesin-encoding gene sabA Finally, we verified that inhibitory lactobacilli reduced H. pylori colonization in an in vivo model. In conclusion, certain Lactobacillus strains affect pathogen adherence by inhibiting sabA expression and thereby reducing H. pylori binding capacity.
authors.affiliation: Department of Molecular Biosciences, The Wenner-Gren Institute, Stockholm University, Stockholm, Sweden.
authors.forename: Nele
authors.initials: N
authors.lastname: de Klerk
authors.affiliation: Department of Molecular Biosciences, The Wenner-Gren Institute, Stockholm University, Stockholm, Sweden.
authors.forename: Lisa
authors.initials: L
authors.lastname: Maudsdotter
authors.affiliation: Department of Molecular Biosciences, The Wenner-Gren Institute, Stockholm University, Stockholm, Sweden.
authors.forename: Hanna
authors.initials: H
authors.lastname: Gebreegziabher
authors.affiliation: Department of Molecular Biosciences, The Wenner-Gren Institute, Stockholm University, Stockholm, Sweden.
authors.forename: Sunil D
authors.initials: SD
authors.lastname: Saroj
authors.affiliation: Department of Molecular Biosciences, The Wenner-Gren Institute, Stockholm University, Stockholm, Sweden.
authors.forename: Beatrice
authors.initials: B
authors.lastname: Eriksson
authors.affiliation: Department of Molecular Biosciences, The Wenner-Gren Institute, Stockholm University, Stockholm, Sweden.
authors.forename: Olaspers Sara
authors.initials: OS
authors.lastname: Eriksson
authors.affiliation: Department of Microbiology, Swedish University of Agricultural Sciences, Uppsala, Sweden.
authors.forename: Stefan
authors.initials: S
authors.lastname: Roos
authors.affiliation: Department of Medical Chemistry and Cell Biology, University of Gothenburg, Gothenburg, Sweden.
authors.forename: Sara
authors.initials: S
authors.lastname: Lindén
authors.affiliation: Department of Molecular Biosciences, The Wenner-Gren Institute, Stockholm University, Stockholm, Sweden.
authors.forename: Hong
authors.initials: H
authors.lastname: Sjölinder
authors.affiliation: Department of Molecular Biosciences, The Wenner-Gren Institute, Stockholm University, Stockholm, Sweden ann-beth.jonsson@su.se.
authors.forename: Ann-Beth
authors.initials: AB
authors.lastname: Jonsson
mesh_terms: D018829:Adhesins, Bacterial / Q000096:biosynthesis*; D000818:Animals; D000898:Antibiosis; D001422:Bacterial Adhesion; D002460:Cell Line; D004195:Disease Models, Animal; D004847:Epithelial Cells / Q000382:microbiology*; D015964:Gene Expression Regulation, Bacterial / Q000187:drug effects; D016481:Helicobacter Infections / Q000382:microbiology / Q000517:prevention & control; D016480:Helicobacter pylori / Q000254:growth & development / Q000502:physiology*; D006801:Humans; D007778:Lactobacillus / Q000254:growth & development / Q000502:physiology*; D008822:Mice, Transgenic
chemical_list: D018829:Adhesins, Bacterial; C500808:SabA protein, Helicobacter pylori