{"id":{"repo_id":"uiuc","oai_identifier":"oai:www.ideals.illinois.edu:2142/99518"},"canonical_url":"https://search.dev.ndltd.org/etd/uiuc/oai:www.ideals.illinois.edu:2142/99518","repository":{"repo_id":"uiuc","name":"University of Illinois - Urbana-Champaign","base_url":"https://www.ideals.illinois.edu/oai-pmh"},"display":{"title":"Influence of chronic Helicobacter pylori infection on systemic and neuroinflammation and its impact on cognition","abstract":"Helicobacter pylori is the major bacterial colonizer of the human stomach. It is estimated that approximately 50% of humans worldwide are chronically infected with this bacterium. Epidemiologically, H. pylori is recognized as the major risk factor and etiological agent of peptic ulcer disease and gastric adenocarcinoma. Most animal models utilized for evaluating H. pylori infection have examined the gastric effects of chronic infection with regard to ulcer and cancer development. However, interest into the potential extra-gastric influences of chronic H. pylori infection has been growing in the field. Utilizing a Sprague-Dawley rat based model for chronic H. pylori infection, the role of chronic infection in the development of systemic and neuro-inflammation was evaluated. High sensitivity ELISA assays were utilized to determine the change in key inflammatory markers locally within the stomach, systemically in the plasma and within the liver and the spleen, and within the central nervous system in the hippocampus and cerebellum. Eradication studies were conducted to determine the causal relationship between H. pylori infection and observed levels of inflammation. Finally, cognitive behavioral studies were conducted to evaluate the potential influence of chronic H. pylori infection on cognitive function and health. Altogether, these studies illustrate a model by which chronic infection established during early life modulates the immune system response to generate a mild, but chronically sustained, systemic and neuro-inflammatory state which is associated with impairment of pre-frontal cortex mediated cognition. Furthermore, it is proposed that the development of these cognitive impairments arise during key developmental windows resulting in persistence of the impairment after successful eradication of H. pylori.","abstract_html":"Helicobacter pylori is the major bacterial colonizer of the human stomach. It is estimated that approximately 50% of humans worldwide are chronically infected with this bacterium. Epidemiologically, H. pylori is recognized as the major risk factor and etiological agent of peptic ulcer disease and gastric adenocarcinoma. Most animal models utilized for evaluating H. pylori infection have examined the gastric effects of chronic infection with regard to ulcer and cancer development. However, interest into the potential extra-gastric influences of chronic H. pylori infection has been growing in the field. Utilizing a Sprague-Dawley rat based model for chronic H. pylori infection, the role of chronic infection in the development of systemic and neuro-inflammation was evaluated. High sensitivity ELISA assays were utilized to determine the change in key inflammatory markers locally within the stomach, systemically in the plasma and within the liver and the spleen, and within the central nervous system in the hippocampus and cerebellum. Eradication studies were conducted to determine the causal relationship between H. pylori infection and observed levels of inflammation. Finally, cognitive behavioral studies were conducted to evaluate the potential influence of chronic H. pylori infection on cognitive function and health. Altogether, these studies illustrate a model by which chronic infection established during early life modulates the immune system response to generate a mild, but chronically sustained, systemic and neuro-inflammatory state which is associated with impairment of pre-frontal cortex mediated cognition. Furthermore, it is proposed that the development of these cognitive impairments arise during key developmental windows resulting in persistence of the impairment after successful eradication of H. pylori.","abstract_has_math":false,"creators":["Reno, Michael L"],"institution":"University of Illinois at Urbana-Champaign","degree_name":"Ph.D.","degree_level":"Dissertation","degree_discipline":"Microbiology","degree_department":null,"school":null,"contributors":["Blanke, Steven R.","Olsen, Gary J.","Mitchell, Douglas A.","Orlean, Peter A.B."],"advisors":[],"committee_chairs":[],"committee_members":[],"year":2018,"date_issued":"2018-03-13T17:35:51Z","date_published":"2018-03-13T17:35:51Z","updated_at":"2026-07-22T22:24:37Z","subjects":["Helicobacter pylori","Inflammation","Cognition"],"languages":["en"],"rights":["Copyright 2017 Michael Llewellyn Reno"],"rights_urls":[],"identifier_entries":[]},"links":{"outbound_url":"http://hdl.handle.net/2142/99518","outbound_label":"Handle","outbound_source":"dc:identifier"},"metadata_groups":[{"id":"people","label":"People","entries":[{"key":"dc:contributor","label":"Contributor","values":["Blanke, Steven R.","Olsen, Gary J.","Mitchell, Douglas A.","Orlean, Peter A.B."]},{"key":"dc:creator","label":"Author","values":["Reno, Michael L"]}]},{"id":"academic_context","label":"Academic Context","entries":[{"key":"dc:date","label":"Dc Date","values":["2018-03-13T17:35:51Z","2020-03-14T09:15:31Z","2017-12-07","2017-12"]},{"key":"dc:type","label":"Dc Type","values":["text"]},{"key":"thesis:degree_discipline","label":"Discipline","values":["Microbiology"]},{"key":"thesis:degree_level","label":"Degree Level","values":["Dissertation"]},{"key":"thesis:degree_name","label":"Degree Name","values":["Ph.D."]},{"key":"thesis:institution_name","label":"Thesis Institution Name","values":["University of Illinois at Urbana-Champaign"]}]},{"id":"subjects_keywords","label":"Subjects and Keywords","entries":[{"key":"dc:subject","label":"Dc Subject","values":["Helicobacter pylori","Inflammation","Cognition"]}]},{"id":"language_rights","label":"Language and Rights","entries":[{"key":"dc:language","label":"Dc Language","values":["en"]},{"key":"dc:rights","label":"Dc Rights","values":["Copyright 2017 Michael Llewellyn Reno"]}]},{"id":"identifiers","label":"Identifiers","entries":[{"key":"dc:identifier","label":"Identifier","values":["http://hdl.handle.net/2142/99518"]}]},{"id":"additional","label":"Additional Metadata","entries":[{"key":"dc:description","label":"Description","values":["Helicobacter pylori is the major bacterial colonizer of the human stomach. It is estimated that approximately 50% of humans worldwide are chronically infected with this bacterium. Epidemiologically, H. pylori is recognized as the major risk factor and etiological agent of peptic ulcer disease and gastric adenocarcinoma. Most animal models utilized for evaluating H. pylori infection have examined the gastric effects of chronic infection with regard to ulcer and cancer development. However, interest into the potential extra-gastric influences of chronic H. pylori infection has been growing in the field. Utilizing a Sprague-Dawley rat based model for chronic H. pylori infection, the role of chronic infection in the development of systemic and neuro-inflammation was evaluated. High sensitivity ELISA assays were utilized to determine the change in key inflammatory markers locally within the stomach, systemically in the plasma and within the liver and the spleen, and within the central nervous system in the hippocampus and cerebellum. Eradication studies were conducted to determine the causal relationship between H. pylori infection and observed levels of inflammation. Finally, cognitive behavioral studies were conducted to evaluate the potential influence of chronic H. pylori infection on cognitive function and health. Altogether, these studies illustrate a model by which chronic infection established during early life modulates the immune system response to generate a mild, but chronically sustained, systemic and neuro-inflammatory state which is associated with impairment of pre-frontal cortex mediated cognition. Furthermore, it is proposed that the development of these cognitive impairments arise during key developmental windows resulting in persistence of the impairment after successful eradication of H. pylori.","Submission published under a 24 month embargo labeled 'Closed Access', the embargo will last until 2019-12-01","The student, Michael Reno, accepted the attached license on 2017-12-06 at 19:17.","The student, Michael Reno, submitted this Dissertation for approval on 2017-12-06 at 19:18.","This Dissertation was approved for publication on 2017-12-07 at 10:38.","DSpace SAF Submission Ingestion Package generated from Vireo submission #11891 on 2018-03-13 at 10:37:52","Made available in DSpace on 2018-03-13T17:35:51Z (GMT). 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It is estimated that approximately 50% of humans worldwide are chronically infected with this bacterium. Epidemiologically, H. pylori is recognized as the major risk factor and etiological agent of peptic ulcer disease and gastric adenocarcinoma. Most animal models utilized for evaluating H. pylori infection have examined the gastric effects of chronic infection with regard to ulcer and cancer development. However, interest into the potential extra-gastric influences of chronic H. pylori infection has been growing in the field. Utilizing a Sprague-Dawley rat based model for chronic H. pylori infection, the role of chronic infection in the development of systemic and neuro-inflammation was evaluated. High sensitivity ELISA assays were utilized to determine the change in key inflammatory markers locally within the stomach, systemically in the plasma and within the liver and the spleen, and within the central nervous system in the hippocampus and cerebellum. Eradication studies were conducted to determine the causal relationship between H. pylori infection and observed levels of inflammation. Finally, cognitive behavioral studies were conducted to evaluate the potential influence of chronic H. pylori infection on cognitive function and health. Altogether, these studies illustrate a model by which chronic infection established during early life modulates the immune system response to generate a mild, but chronically sustained, systemic and neuro-inflammatory state which is associated with impairment of pre-frontal cortex mediated cognition. Furthermore, it is proposed that the development of these cognitive impairments arise during key developmental windows resulting in persistence of the impairment after successful eradication of H. pylori.","Submission published under a 24 month embargo labeled 'Closed Access', the embargo will last until 2019-12-01","The student, Michael Reno, accepted the attached license on 2017-12-06 at 19:17.","The student, Michael Reno, submitted this Dissertation for approval on 2017-12-06 at 19:18.","This Dissertation was approved for publication on 2017-12-07 at 10:38.","DSpace SAF Submission Ingestion Package generated from Vireo submission #11891 on 2018-03-13 at 10:37:52","Made available in DSpace on 2018-03-13T17:35:51Z (GMT). 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