Host cell adhesion of Trichomonas vaginalis is down-modulated by Lactobacillus gasseri with the contribution of an aggregation-promoting factor-like protein

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dc.contributor.advisor Simoes-Barbosa, A en
dc.contributor.author Phukan, Niha en
dc.date.accessioned 2017-04-05T00:37:44Z en
dc.date.issued 2016 en
dc.identifier.uri http://hdl.handle.net/2292/32461 en
dc.description.abstract Trichomonas vaginalis is a sexually transmitted protozoan parasite that colonises the human urogenital tract. It is the causative organism of trichomoniasis, the most common non-viral sexually transmitted infection worldwide. Being an extracellular parasite, adhesion to the vaginal epithelial cell layer is a pre-requisite for successful infection establishment. However once inside the vagina, T. vaginalis is likely to face competition by the residual lactobacilli. Studies have shown that the vaginal lactobacilli are host protective and capable of mitigating pathogens to varying degrees. This observation indicates that the role played by the indigenous lactobacilli is influential in determining infection outcomes. Current knowledge on the Trichomonas-Lactobacillus interaction process is, however, very limited. This work advances our understanding of this microbial interaction, particularly how vaginal lactobacilli affect the adhesion of the Trichomonas parasite to human cells. In order to achieve this, multiple adhesion assays were performed where the host vaginal ectocervical cells were pre-incubated with lactobacilli, followed by Trichomonas incubation. Unbound cells were washed away and the adherent T. vaginalis cells were finally counted using a flow cytometer. Our findings reveal that the lactobacilli can utilise several mechanisms to reduce the adhesion of Trichomonas to human cells. These mechanisms include cell aggregation, competition for binding sites, exclusion of parasites and physical blocking of the attachment sites. Using a series of fractionation and chemical/enzymatic treatments, we have shown that molecules present on the surface of the Lactobacillus gasseri cells contribute to this inhibitory phenotype. Non-covalently associated proteins on the surface of this bacterium was found to play an important role and at least one of its aggregation-promoting factor-like proteins was proved to be involved in T. vaginalis adhesion inhibition. Heterologous expression of this protein in Lactococcus lactis increased its ability to inhibit parasitic attachment to host cells despite not affecting other bacterial properties, such as aggregation and host cell adhesion. This work highlights the role that our microbiota plays in the maintenance of vaginal health. The understanding of how these two microbes interact with each other and compete in the vagina along with the discovery of molecules involved in this interaction process can pave the way for the development of novel treatments and drugs against trichomoniasis. en
dc.publisher ResearchSpace@Auckland en
dc.relation.ispartof PhD Thesis - University of Auckland en
dc.relation.isreferencedby UoA99264906303202091 en
dc.rights Items in ResearchSpace are protected by copyright, with all rights reserved, unless otherwise indicated. Previously published items are made available in accordance with the copyright policy of the publisher. en
dc.rights.uri https://researchspace.auckland.ac.nz/docs/uoa-docs/rights.htm en
dc.rights.uri http://creativecommons.org/licenses/by-nc-nd/3.0/nz/ en
dc.title Host cell adhesion of Trichomonas vaginalis is down-modulated by Lactobacillus gasseri with the contribution of an aggregation-promoting factor-like protein en
dc.type Thesis en
thesis.degree.discipline Biological Sciences en
thesis.degree.grantor The University of Auckland en
thesis.degree.level Doctoral en
thesis.degree.name PhD en
dc.rights.holder Copyright: The author en
dc.rights.accessrights http://purl.org/eprint/accessRights/OpenAccess en
pubs.elements-id 621011 en
pubs.record-created-at-source-date 2017-04-05 en


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