title: Lactobacilli require physical contact to reduce staphylococcal TSST-1 secretion and vaginal epithelial inflammatory response.
abstract: ITALIC! Staphylococcus aureusbiofilms can be found on vaginal epithelia, secreting toxins and causing inflammation. The co-vaginal species ITALIC! Lactobacilluscan alter staphylococcal-induced epithelial secretion of inflammatory cytokines and quench staphylococcal toxic shock syndrome toxin-1 secretion. It is hypothesized that these effects of lactobacilli require direct physical contact between lactobacilli, staphylococci and the epithelium. Indeed, lactobacilli only reduced ITALIC! S. aureus-induced inflammatory cytokine expression when allowed physical contact with vaginal epithelial cells. Furthermore, a reduction in toxic shock syndrome toxin-1 secretion only occurred when a probiotic ITALIC! Lactobacillusstrain was allowed contact, but not when being physically separated from ITALIC! S. aureus Bacterial-probe atomic force microscopy demonstrated that lactobacilli and staphylococci strongly adhere to epithelial cells, while lactobacilli adhere stronger to staphylococci than staphylococci to each other, giving lactobacilli opportunity to penetrate and reside in staphylococcal biofilms, as visualized using confocal laser scanning microscopy with fluorescence ITALIC! in situhybridization probes. These results identify that physical contact and biochemical signaling by lactobacilli are intrinsically linked mechanisms that reduce virulence of ITALIC! S. aureusbiofilm.
authors.affiliation: University of Groningen and University Medical Center Groningen, Department of BioMedical Engineering, Antonius Deusinglaan 1, 9713 AV Groningen, the Netherlands.
authors.forename: Jessica A
authors.initials: JA
authors.lastname: Younes
authors.affiliation: Human Microbiology and Probiotics, Lawson Health Research Institute, 268 Grosvenor Street, London, Ontario, N6A 4V2, Canada Departments of Microbiology and Immunology, and Surgery, The University of Western Ontario, London, Ontario, N6A 5C1, Canada.
authors.forename: Gregor
authors.initials: G
authors.lastname: Reid
authors.affiliation: University of Groningen and University Medical Center Groningen, Department of BioMedical Engineering, Antonius Deusinglaan 1, 9713 AV Groningen, the Netherlands h.c.van.der.mei@umcg.nl.
authors.forename: Henny C
authors.initials: HC
authors.lastname: van der Mei
authors.affiliation: University of Groningen and University Medical Center Groningen, Department of BioMedical Engineering, Antonius Deusinglaan 1, 9713 AV Groningen, the Netherlands.
authors.forename: Henk J
authors.initials: HJ
authors.lastname: Busscher
mesh_terms: D001422:Bacterial Adhesion; D001427:Bacterial Toxins; D002460:Cell Line; D016207:Cytokines / Q000378:metabolism; D004768:Enterotoxins / Q000378:metabolism*; D004847:Epithelial Cells; D005260:Female; D006801:Humans; D018836:Inflammation Mediators / Q000378:metabolism; D007778:Lactobacillus / Q000502:physiology*; D056265:Microbial Interactions; D013211:Staphylococcus aureus / Q000502:physiology*; D018089:Superantigens; D016585:Vaginosis, Bacterial / Q000378:metabolism / Q000382:microbiology
chemical_list: D001427:Bacterial Toxins; D016207:Cytokines; D004768:Enterotoxins; D018836:Inflammation Mediators; D018089:Superantigens; C030107:enterotoxin F, Staphylococcal
keywords: Lactobacillus jenseii; Lactobacillus reuteri; cytokine secretion; probiotic; quorum quencing; toxic shock syndrome toxin-1