Massachusetts Institute of Technology
Pathogenesis of the carcinogenic bacterium, Helicobacter pylori
Abstract
dc:description.abstractGastric cancer is the second most common malignancy in the digestive system and the second leading cause of cancer-related death worldwide. Epidemiological data and experimental studies have identified several risk factors for gastric cancer, including Helicobacter pylori infection, low fruit and vegetable intake, N-nitrosoamine exposure, high salt diet, and smoking. Among these risk factors, H. pylori infection is the major cause of gastric cancer. Therefore, H. pylori has been classified as a type 1 (definite) carcinogen for gastric cancer by the World Health Organization (WHO) in 1994. H. pylori colonizes the human stomach and has been definitively linked to chronic gastritis. Infection in some: susceptible individuals results in serious gastric disease such as peptic ulcer or gastric cancer. The first aim of this thesis was to examine the role of different T cell subpopulations in H. pylori gastritis. Using a murine adoptive transfer model, adoptive transfer of wildtype (wt) effector T cells (TE) into H. pylori-infected lymphopenic Rag2-/- recipient mice resulted in H. pylori-associated corpus gastritis superimposed with non-specific gastroduodenitis. Cotransfer with TE and regulatory T cells (TR) from wt or IL10-/- mice reduced gastroduodenitis, but only wt TR cells reduced corpus gastritis.
Degree
thesis:*- Department dc:contributor.department
- Massachusetts Institute of Technology. Biological Engineering Division.
- Grantor dc:publisher
- Massachusetts Institute of Technology
- Year dc:date.issued
- 2007
Author and committee
dc:creator, dc:contributor.*- Author dc:creator
-
- Lee, Chung-Wei, Ph. D. Massachusetts Institute of Technology
- Advisor dc:contributor.advisor
-
- James G. Fox.
Subjects
dc:subject × 1Rights
dc:rights- Statement dc:rights
-
- MIT theses are protected by copyright. They may be viewed, downloaded, or printed from this source but further reproduction or distribution in any format is prohibited without written permission.
- Licence dc:rights.uri
- Language dc:language.iso
- eng
Identifiers
dc:identifier.*- Identifier URI
- http://dspace.mit.edu/handle/1721.1/39909
- OAI identifier oai:identifier
- oai:dspace.mit.edu:1721.1/39909