Please use this identifier to cite or link to this item: http://scholarbank.nus.edu.sg/handle/10635/79520
Title: BLASTOCYSTIS: INVESTIGATION OF PARASITE ADHESION AND ITS ROLE IN MEDIATING INTESTINAL BARRIER COMPROMISE
Authors: WU ZHAONA
Keywords: Blastocystis, adhesion, pathogenesis, barrier dysfunction, galactose-binding protein, fitness cost
Issue Date: 20-Jan-2014
Source: WU ZHAONA (2014-01-20). BLASTOCYSTIS: INVESTIGATION OF PARASITE ADHESION AND ITS ROLE IN MEDIATING INTESTINAL BARRIER COMPROMISE. ScholarBank@NUS Repository.
Abstract: Blastocystis is an emerging protistan pathogen commonly found in the human gut. Despite significant advances made regarding its pathobiology, major gaps remain unfilled. Adhesion of Blastocystis to host cells, as the first step to establish colonic infection, has never been investigated. The aim of this study was to investigate the pathobiology of Blastocystis adhesion. An extensive analysis of extrinsic and intrinsic factors influencing host-parasite adhesion revealed that galactose-binding protein on the surface of the parasite was important in mediating parasite attachment. Pathogenic effects on the host cells following attachment of Blastocystis were characterized and it was shown that intra- and inter-subtype variations in cytopathogenicity were largely dependent on their adhesive properties. Altogether, the findings from the study identified the importance of adhesion in Blastocystis pathogenesis, advanced our understanding of in the mechanism of attachment and also pointed towards new directions for therapeutic interventions targeting adhesion in Blastocystis infections.
URI: http://scholarbank.nus.edu.sg/handle/10635/79520
Appears in Collections:Ph.D Theses (Open)

Show full item record
Files in This Item:
File Description SizeFormatAccess SettingsVersion 
Wu ZN.pdf6.5 MBAdobe PDF

OPEN

NoneView/Download

Page view(s)

90
checked on Jan 19, 2018

Download(s)

78
checked on Jan 19, 2018

Google ScholarTM

Check


Items in DSpace are protected by copyright, with all rights reserved, unless otherwise indicated.