Helicobacter pylori is a gram-negative bacterium that infects half the world population and is the etiological cause of numerous gastric pathologies. H. pylori possess numerous mechanisms to promote its survival and modulate host immunity. We propose that H. pylori can modulate intercellular communication by manipulating the host exosome pathway. Exosomes are secreted nanovesicles that contain different proteins and microRNAs that can be transferred between cells to alter cell signaling and gene expression. We demonstrate that H. pylori infection increases host exosome secretion. Furthermore, infection can alter exosome composition as VacA, a bacterial virulence factor, can be exported in exosomes and Argonaute 5, a miRNA effector protein, is upregulated in exosomes during infection. Lastly, we show preliminary evidence that infection-modulated exosomes can modulate immune-regulatory signaling in dendritic cells by activating STAT3. Together, these studies elucidate a novel mechanism by which H. pylori can modulate the host environment and promote its continued survival.
| Identifer | oai:union.ndltd.org:TORONTO/oai:tspace.library.utoronto.ca:1807/43343 |
| Date | 11 December 2013 |
| Creators | Wu, Ted Chia Hao |
| Contributors | Jones, Nicola L. |
| Source Sets | University of Toronto |
| Language | en_ca |
| Detected Language | English |
| Type | Thesis |
Page generated in 0.0022 seconds