{"id":{"repo_id":"mo-state","oai_identifier":"oai:bearworks.missouristate.edu:theses-2282"},"canonical_url":"https://search.dev.ndltd.org/etd/mo-state/oai:bearworks.missouristate.edu:theses-2282","repository":{"repo_id":"mo-state","name":"Missouri State University","base_url":"https://bearworks.missouristate.edu/do/oai/"},"display":{"title":"Regulation of Synergistic Inducible ABIN-3 Gene Expression in Response to IL-10 and LPS","abstract":"Macrophages play an important role in the sensing of microbial infection and initiating innate immune responses. The activation of macrophages by pro-inflammatory stimuli, such as bacterial LPS, is mediated through changes in the expression of genes that function to promote inflammation. Pro-inflammatory signaling and gene expression is tightly regulated through the parallel induction of anti-inflammatory genes in response to the host cytokine Interleukin-10 (IL-10). The mechanisms by which IL-10 acts to restrain pro-inflammatory signaling remain incompletely defined. Previously, we identified ABIN-3 as an IL-10-inducible gene capable of inhibiting the action of the pro-inflammatory transcription factor NF-κB in human macrophages. Interestingly, IL-10 can induce expression of ABIN-3 only in macrophages concurrently responding to LPS. Herein, I present studies into the mechanism by which IL-10 synergizes with LPS to induce ABIN-3 gene expression. ABIN-3 falls into the category of a secondary response gene requiring new protein synthesis for its induction in response to IL-10 and LPS. I examined whether the induction of ABIN-3 expression is regulated at the level of transcription or at a post-transcriptional level involving an increase in its mRNA stability. These data indicate that IL-10 synergizes with LPS to induce ABIN-3 gene transcription as opposed to inducing stabilization of its mRNA. Future studies will aim to determine the minimal cis-acting elements within the ABIN-3 gene responsible for its induction by both IL-10 and LPS. These studies should ultimately lead to a better understanding of the crosstalk mechanisms between anti- and pro-inflammatory signaling pathways.","abstract_html":"Macrophages play an important role in the sensing of microbial infection and initiating innate immune responses. The activation of macrophages by pro-inflammatory stimuli, such as bacterial LPS, is mediated through changes in the expression of genes that function to promote inflammation. Pro-inflammatory signaling and gene expression is tightly regulated through the parallel induction of anti-inflammatory genes in response to the host cytokine Interleukin-10 (IL-10). The mechanisms by which IL-10 acts to restrain pro-inflammatory signaling remain incompletely defined. Previously, we identified ABIN-3 as an IL-10-inducible gene capable of inhibiting the action of the pro-inflammatory transcription factor NF-κB in human macrophages. Interestingly, IL-10 can induce expression of ABIN-3 only in macrophages concurrently responding to LPS. Herein, I present studies into the mechanism by which IL-10 synergizes with LPS to induce ABIN-3 gene expression. ABIN-3 falls into the category of a secondary response gene requiring new protein synthesis for its induction in response to IL-10 and LPS. I examined whether the induction of ABIN-3 expression is regulated at the level of transcription or at a post-transcriptional level involving an increase in its mRNA stability. These data indicate that IL-10 synergizes with LPS to induce ABIN-3 gene transcription as opposed to inducing stabilization of its mRNA. Future studies will aim to determine the minimal cis-acting elements within the ABIN-3 gene responsible for its induction by both IL-10 and LPS. These studies should ultimately lead to a better understanding of the crosstalk mechanisms between anti- and pro-inflammatory signaling pathways.","abstract_has_math":false,"creators":["Peterson, Brian A."],"institution":null,"degree_name":"Master of Science in Biology","degree_level":"Masters","degree_discipline":"Biology","degree_department":null,"school":null,"contributors":["Brian Weaver"],"advisors":[],"committee_chairs":[],"committee_members":[],"year":2010,"date_issued":"2010-05-01T07:00:00Z","date_published":"2010-05-01T07:00:00Z","updated_at":"2026-07-24T03:16:17Z","subjects":["innate immunity","inflammation","IL-10","LPS","ABIN-3","Biology"],"languages":[],"rights":["© Brian A. Peterson"],"rights_urls":[],"identifier_entries":[]},"links":{"outbound_url":"https://bearworks.missouristate.edu/theses/1281","outbound_label":"Repository record","outbound_source":"dc:identifier"},"metadata_groups":[{"id":"people","label":"People","entries":[{"key":"dc:contributor","label":"Contributor","values":["Brian Weaver"]},{"key":"dc:creator","label":"Author","values":["Peterson, Brian A."]}]},{"id":"academic_context","label":"Academic Context","entries":[{"key":"thesis:degree_discipline","label":"Discipline","values":["Biology"]},{"key":"thesis:degree_level","label":"Degree Level","values":["Masters"]},{"key":"thesis:degree_name","label":"Degree Name","values":["Master of Science in Biology"]}]},{"id":"subjects_keywords","label":"Subjects and Keywords","entries":[{"key":"dc:subject","label":"Dc Subject","values":["innate immunity","inflammation","IL-10","LPS","ABIN-3","Biology"]}]},{"id":"language_rights","label":"Language and Rights","entries":[{"key":"dc:rights","label":"Dc Rights","values":["© Brian A. Peterson"]}]},{"id":"identifiers","label":"Identifiers","entries":[{"key":"dc:identifier","label":"Identifier","values":["https://bearworks.missouristate.edu/theses/1281"]}]},{"id":"additional","label":"Additional Metadata","entries":[{"key":"dc:description.abstract","label":"Abstract","values":["Macrophages play an important role in the sensing of microbial infection and initiating innate immune responses. The activation of macrophages by pro-inflammatory stimuli, such as bacterial LPS, is mediated through changes in the expression of genes that function to promote inflammation. Pro-inflammatory signaling and gene expression is tightly regulated through the parallel induction of anti-inflammatory genes in response to the host cytokine Interleukin-10 (IL-10). The mechanisms by which IL-10 acts to restrain pro-inflammatory signaling remain incompletely defined. Previously, we identified ABIN-3 as an IL-10-inducible gene capable of inhibiting the action of the pro-inflammatory transcription factor NF-κB in human macrophages. Interestingly, IL-10 can induce expression of ABIN-3 only in macrophages concurrently responding to LPS. Herein, I present studies into the mechanism by which IL-10 synergizes with LPS to induce ABIN-3 gene expression. ABIN-3 falls into the category of a secondary response gene requiring new protein synthesis for its induction in response to IL-10 and LPS. I examined whether the induction of ABIN-3 expression is regulated at the level of transcription or at a post-transcriptional level involving an increase in its mRNA stability. These data indicate that IL-10 synergizes with LPS to induce ABIN-3 gene transcription as opposed to inducing stabilization of its mRNA. Future studies will aim to determine the minimal cis-acting elements within the ABIN-3 gene responsible for its induction by both IL-10 and LPS. These studies should ultimately lead to a better understanding of the crosstalk mechanisms between anti- and pro-inflammatory signaling pathways."]},{"key":"dc:title","label":"Title","values":["Regulation of Synergistic Inducible ABIN-3 Gene Expression in Response to IL-10 and LPS"]}]}],"canonical_facts":{"dc:contributor":["Brian Weaver"],"dc:creator":["Peterson, Brian A."],"dc:description.abstract":["Macrophages play an important role in the sensing of microbial infection and initiating innate immune responses. The activation of macrophages by pro-inflammatory stimuli, such as bacterial LPS, is mediated through changes in the expression of genes that function to promote inflammation. Pro-inflammatory signaling and gene expression is tightly regulated through the parallel induction of anti-inflammatory genes in response to the host cytokine Interleukin-10 (IL-10). The mechanisms by which IL-10 acts to restrain pro-inflammatory signaling remain incompletely defined. Previously, we identified ABIN-3 as an IL-10-inducible gene capable of inhibiting the action of the pro-inflammatory transcription factor NF-κB in human macrophages. Interestingly, IL-10 can induce expression of ABIN-3 only in macrophages concurrently responding to LPS. Herein, I present studies into the mechanism by which IL-10 synergizes with LPS to induce ABIN-3 gene expression. ABIN-3 falls into the category of a secondary response gene requiring new protein synthesis for its induction in response to IL-10 and LPS. I examined whether the induction of ABIN-3 expression is regulated at the level of transcription or at a post-transcriptional level involving an increase in its mRNA stability. These data indicate that IL-10 synergizes with LPS to induce ABIN-3 gene transcription as opposed to inducing stabilization of its mRNA. Future studies will aim to determine the minimal cis-acting elements within the ABIN-3 gene responsible for its induction by both IL-10 and LPS. These studies should ultimately lead to a better understanding of the crosstalk mechanisms between anti- and pro-inflammatory signaling pathways."],"dc:identifier":["https://bearworks.missouristate.edu/theses/1281"],"dc:rights":["© Brian A. Peterson"],"dc:subject":["innate immunity","inflammation","IL-10","LPS","ABIN-3","Biology"],"dc:title":["Regulation of Synergistic Inducible ABIN-3 Gene Expression in Response to IL-10 and LPS"],"thesis:degree_discipline":["Biology"],"thesis:degree_level":["Masters"],"thesis:degree_name":["Master of Science in Biology"]},"updated_at":"2026-07-24T03:16:17Z"}