{"id":{"repo_id":"utmb","oai_identifier":"oai:utmb-ir.tdl.org:2152.3/724"},"canonical_url":"https://search.dev.ndltd.org/etd/utmb/oai:utmb-ir.tdl.org:2152.3/724","repository":{"repo_id":"utmb","name":"University of Texas Medical Branch","base_url":"https://utmb-ir.tdl.org/server/oai/request"},"display":{"title":"Expression of interleukin-16 in gastric mucosa: a possible role in the persistance of helicobacter pylori infection","abstract":"Helicobacter pylori (H. pylori) infects the human gastric mucosa of >50% of humankind and causes chronic gastritis, peptic ulcers, and gastric adenocarcinoma. H. pylori infected gastric epithelial cells (GECs) produce an array of chemokines that recruit other cells. IL-16 is potentially a key chemokine not yet examined during H. pylori infection. IL-16 selectively recruits CD4+ T cells since it uses CD4 as a receptor; but makes them unresponsive to antigen, which could explain failed vaccine clinical trials. As T cells from the H. pylori-infected gastric mucosa are hyporesponsive, I wanted to investigate the production of IL-16 by GECs, the mechanisms underlying IL-16 production and the role of gastric IL-16 in the persistent of H. pylori-infection. IL-16 expression by GECs was analyzed using FACS and RT-PCR following infection with H. pylori as well as mediators present during infection. I observed that H. pylori increases expression of IL-16 in different gastric epithelial cell lines. Also, histamine, IL-8 and IFN- increased IL-16 expression. These findings uncover relevant information pertaining to the accumulation of CD4+ T cells that is observed in patients’ gastric mucosa with H. pylori and could explain why clinical trials have failed in efforts to develop a vaccine to this important pathogen.","abstract_html":"Helicobacter pylori (H. pylori) infects the human gastric mucosa of >50% of humankind and causes chronic gastritis, peptic ulcers, and gastric adenocarcinoma. H. pylori infected gastric epithelial cells (GECs) produce an array of chemokines that recruit other cells. IL-16 is potentially a key chemokine not yet examined during H. pylori infection. IL-16 selectively recruits CD4+ T cells since it uses CD4 as a receptor; but makes them unresponsive to antigen, which could explain failed vaccine clinical trials. As T cells from the H. pylori-infected gastric mucosa are hyporesponsive, I wanted to investigate the production of IL-16 by GECs, the mechanisms underlying IL-16 production and the role of gastric IL-16 in the persistent of H. pylori-infection. IL-16 expression by GECs was analyzed using FACS and RT-PCR following infection with H. pylori as well as mediators present during infection. I observed that H. pylori increases expression of IL-16 in different gastric epithelial cell lines. Also, histamine, IL-8 and IFN- increased IL-16 expression. These findings uncover relevant information pertaining to the accumulation of CD4+ T cells that is observed in patients’ gastric mucosa with H. pylori and could explain why clinical trials have failed in efforts to develop a vaccine to this important pathogen.","abstract_has_math":false,"creators":["Alzahrani, Shatha A"],"institution":"The University of Texas Medical Branch at Galveston","degree_name":"Microbiology and Immunology (Masters)","degree_level":"Masters","degree_discipline":"Immunology","degree_department":null,"school":null,"contributors":[],"advisors":["Reyes, Victor"],"committee_chairs":[],"committee_members":["PINCHUK, Iryna","MIDORO-HORIUTI, TERUMI"],"year":null,"date_issued":"","date_published":null,"updated_at":"2026-07-24T05:51:09Z","subjects":["H. pylori","Gastric Epithelial Cells, Interleukin-16."],"languages":[],"rights":[],"rights_urls":[],"identifier_entries":[]},"links":{"outbound_url":"http://hdl.handle.net/2152.3/724","outbound_label":"Handle","outbound_source":"dc:identifier.uri"},"metadata_groups":[{"id":"people","label":"People","entries":[{"key":"dc:contributor.advisor","label":"Advisor","values":["Reyes, Victor"]},{"key":"dc:contributor.committeemember","label":"Committee Member","values":["PINCHUK, Iryna","MIDORO-HORIUTI, TERUMI"]},{"key":"dc:creator","label":"Author","values":["Alzahrani, Shatha A"]}]},{"id":"academic_context","label":"Academic Context","entries":[{"key":"dc:date.accessioned","label":"Dc Date Accessioned","values":["2016-05-05T21:54:22Z"]},{"key":"dc:date.available","label":"Dc Date Available","values":["2016-05-05T21:54:22Z"]},{"key":"dc:type","label":"Dc Type","values":["Thesis"]},{"key":"thesis:degree_discipline","label":"Discipline","values":["Immunology"]},{"key":"thesis:degree_level","label":"Degree Level","values":["Masters"]},{"key":"thesis:degree_name","label":"Degree Name","values":["Microbiology and Immunology (Masters)"]},{"key":"thesis:institution_name","label":"Thesis Institution Name","values":["The University of Texas Medical Branch at Galveston"]}]},{"id":"subjects_keywords","label":"Subjects and Keywords","entries":[{"key":"dc:subject","label":"Dc Subject","values":["H. pylori","Gastric Epithelial Cells, Interleukin-16."]}]},{"id":"identifiers","label":"Identifiers","entries":[{"key":"dc:identifier.uri","label":"Identifier URI","values":["http://hdl.handle.net/2152.3/724"]}]},{"id":"additional","label":"Additional Metadata","entries":[{"key":"dc:description.abstract","label":"Abstract","values":["Helicobacter pylori (H. pylori) infects the human gastric mucosa of >50% of humankind and causes chronic gastritis, peptic ulcers, and gastric adenocarcinoma. H. pylori infected gastric epithelial cells (GECs) produce an array of chemokines that recruit other cells. IL-16 is potentially a key chemokine not yet examined during H. pylori infection. IL-16 selectively recruits CD4+ T cells since it uses CD4 as a receptor; but makes them unresponsive to antigen, which could explain failed vaccine clinical trials. As T cells from the H. pylori-infected gastric mucosa are hyporesponsive, I wanted to investigate the production of IL-16 by GECs, the mechanisms underlying IL-16 production and the role of gastric IL-16 in the persistent of H. pylori-infection. IL-16 expression by GECs was analyzed using FACS and RT-PCR following infection with H. pylori as well as mediators present during infection. I observed that H. pylori increases expression of IL-16 in different gastric epithelial cell lines. Also, histamine, IL-8 and IFN- increased IL-16 expression. These findings uncover relevant information pertaining to the accumulation of CD4+ T cells that is observed in patients’ gastric mucosa with H. pylori and could explain why clinical trials have failed in efforts to develop a vaccine to this important pathogen."]},{"key":"dc:format.mimetype","label":"Dc Format Mimetype","values":["application/pdf"]},{"key":"dc:title","label":"Title","values":["Expression of interleukin-16 in gastric mucosa: a possible role in the persistance of helicobacter pylori infection"]}]}],"canonical_facts":{"dc:contributor.advisor":["Reyes, Victor"],"dc:contributor.committeemember":["PINCHUK, Iryna","MIDORO-HORIUTI, TERUMI"],"dc:creator":["Alzahrani, Shatha A"],"dc:date.accessioned":["2016-05-05T21:54:22Z"],"dc:date.available":["2016-05-05T21:54:22Z"],"dc:description.abstract":["Helicobacter pylori (H. pylori) infects the human gastric mucosa of >50% of humankind and causes chronic gastritis, peptic ulcers, and gastric adenocarcinoma. H. pylori infected gastric epithelial cells (GECs) produce an array of chemokines that recruit other cells. IL-16 is potentially a key chemokine not yet examined during H. pylori infection. IL-16 selectively recruits CD4+ T cells since it uses CD4 as a receptor; but makes them unresponsive to antigen, which could explain failed vaccine clinical trials. As T cells from the H. pylori-infected gastric mucosa are hyporesponsive, I wanted to investigate the production of IL-16 by GECs, the mechanisms underlying IL-16 production and the role of gastric IL-16 in the persistent of H. pylori-infection. IL-16 expression by GECs was analyzed using FACS and RT-PCR following infection with H. pylori as well as mediators present during infection. I observed that H. pylori increases expression of IL-16 in different gastric epithelial cell lines. Also, histamine, IL-8 and IFN- increased IL-16 expression. 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