Year: 2012
Type: dissertation
Abstract: Helicobacter pylori infects the human gastric mucosa and induces a chronic gastritis that does not eliminate the pathogen. H. pylori infection is the primary risk factor for gastric cancer development. The host immune system is crucial for both bacterial elimination and tumor surveillance. The interaction between H. pylori and dendritic cells (DC), key orchestrators of the host immune response, was examined. H. pylori activated the Signal Transducer and Activator of Transcription 3 (STAT3) pathway, assayed using immunoblotting, in bone marrow-derived DCs. This blunted DC maturation, determined by CD86 and MHC II expression, in an autocrine/paracrine IL-10-dependent pathway. H. pylori infection stimulated the production of cytokines including IL-10, IL-12p40, and TNF-α as determined using ELISA and multiplex analysis. DC co-culture with T cells did not drive regulatory T cell development. These results demonstrate that H. pylori blunts DC maturation, which may play an important role in promoting bacterial persistence and disease.
Source: TSpace (University of Toronto)
Author: David Rizzuti
Language: English
Subfield: Gastroenterology
Field: Medicine
Domain: Health Sciences
Open Access status: green
OpenAlex ID: W2762200807