{"id":{"repo_id":"utmb","oai_identifier":"oai:utmb-ir.tdl.org:2152.3/40"},"canonical_url":"https://search.dev.ndltd.org/etd/utmb/oai:utmb-ir.tdl.org:2152.3/40","repository":{"repo_id":"utmb","name":"University of Texas Medical Branch","base_url":"https://utmb-ir.tdl.org/server/oai/request"},"display":{"title":"Anthrax toxin effects on B lymphocyte function","abstract":"Bacillus anthracis is a gram-positive spore-forming rod capable of causing cutaneous, gastrointestinal and inhalational anthrax. It has a number of virulence factors of which, the two toxins are of great importance. Lethal toxin is a zinc metaloprotease that cleaves the N terminus of the mitogen-activated protein kinase (MAPK) kinase family 1-7, with the exception of MEK5. This kinase family is responsible for activating the mitogen-activated protein kinase (MAPK) cascade. This cascade includes extracellular signal-regulated protein kinases (ERK), c-Jun NH2-terminal kinases (JNK) and p38 kinases. The disruption of these signaling pathways has a number of deleterious downstream effects that vary by cell type. Edema factor is a powerful calmodulin-dependent adenylyl cyclase that forms 3’,5’-adenosine monophosphate (cAMP) from adenosine triphosphate (ATP). This enzymatic reaction causes an increase in intracellular cyclic AMP (cAMP) in host cells. As cAMP is a prominent second messenger in cellular signaling, edema toxin has a wide array of effects on numerous cell types and functions. \\r\\nTo determine the effects of the anthrax toxins on the adaptive immune response, B lymphocytes were exposed to LeTx or EdTx in vitro. LeTx and EdTx both inhibit B cell activation in different manners. LeTx inhibited B cell proliferation but not migration, while EdTx inhibited B cell migration but not proliferation. LeTx and EdTx altered expression patterns of B cell activation markers. EdTx inhibited MIP-1α and MIP-1β while enhancing IL-6 production. Previously unseen in any cell type EdTx was demonstrated to be cytotoxic to naïve B cells.\\r\\nThe research presented in this report illustrates the inhibitory effects of LeTx and EdTx on B lymphocytes, providing valuable insight into the immunoevasion tactics of B. anthracis.\\r\\n","abstract_html":"Bacillus anthracis is a gram-positive spore-forming rod capable of causing cutaneous, gastrointestinal and inhalational anthrax. It has a number of virulence factors of which, the two toxins are of great importance. Lethal toxin is a zinc metaloprotease that cleaves the N terminus of the mitogen-activated protein kinase (MAPK) kinase family 1-7, with the exception of MEK5. This kinase family is responsible for activating the mitogen-activated protein kinase (MAPK) cascade. This cascade includes extracellular signal-regulated protein kinases (ERK), c-Jun NH2-terminal kinases (JNK) and p38 kinases. The disruption of these signaling pathways has a number of deleterious downstream effects that vary by cell type. Edema factor is a powerful calmodulin-dependent adenylyl cyclase that forms 3’,5’-adenosine monophosphate (cAMP) from adenosine triphosphate (ATP). This enzymatic reaction causes an increase in intracellular cyclic AMP (cAMP) in host cells. As cAMP is a prominent second messenger in cellular signaling, edema toxin has a wide array of effects on numerous cell types and functions. \\r\\nTo determine the effects of the anthrax toxins on the adaptive immune response, B lymphocytes were exposed to LeTx or EdTx in vitro. LeTx and EdTx both inhibit B cell activation in different manners. LeTx inhibited B cell proliferation but not migration, while EdTx inhibited B cell migration but not proliferation. LeTx and EdTx altered expression patterns of B cell activation markers. EdTx inhibited MIP-1α and MIP-1β while enhancing IL-6 production. Previously unseen in any cell type EdTx was demonstrated to be cytotoxic to naïve B cells.\\r\\nThe research presented in this report illustrates the inhibitory effects of LeTx and EdTx on B lymphocytes, providing valuable insight into the immunoevasion tactics of B. anthracis.\\r\\n","abstract_has_math":false,"creators":["Bryan Thomas Gnade"],"institution":"The University of Texas Medical Branch","degree_name":"PhD","degree_level":"Doctoral","degree_discipline":null,"degree_department":null,"school":null,"contributors":[],"advisors":["Johnny Peterson"],"committee_chairs":[],"committee_members":["Rolf Konig","Gustavo Valbuena","David Craft"],"year":2010,"date_issued":"2010-01-11","date_published":"2010-01-11","updated_at":"2026-07-24T05:51:10Z","subjects":["lethal toxin","edema toxin","bacillus anthracis","B cell","anthrax toxin","anthrax"],"languages":["eng"],"rights":["Copyright © is held by the author. Presentation of this material on the TDL web site by The University of Texas Medical Branch at Galveston was made possible under a limited license grant from the author who has retained all copyrights in the works."],"rights_urls":[],"identifier_entries":[{"key":"dc:identifier.other","label":"Dc Identifier Other","values":["etd-03112010-180727"],"render_values":[{"text":"etd-03112010-180727","href":null,"code":true}]}]},"links":{"outbound_url":"http://hdl.handle.net/2152.3/40","outbound_label":"Handle","outbound_source":"dc:identifier.uri"},"metadata_groups":[{"id":"people","label":"People","entries":[{"key":"dc:contributor.advisor","label":"Advisor","values":["Johnny Peterson"]},{"key":"dc:contributor.committeemember","label":"Committee Member","values":["Rolf Konig","Gustavo Valbuena","David Craft"]},{"key":"dc:creator","label":"Author","values":["Bryan Thomas Gnade"]}]},{"id":"academic_context","label":"Academic Context","entries":[{"key":"dc:date.accessioned","label":"Dc Date Accessioned","values":["2011-12-20T16:04:17Z"]},{"key":"dc:date.available","label":"Dc Date Available","values":["2010-09-28","2011-12-20T16:04:17Z"]},{"key":"dc:date.issued","label":"Date","values":["2010-01-11"]},{"key":"thesis:degree_level","label":"Degree Level","values":["Doctoral"]},{"key":"thesis:degree_name","label":"Degree Name","values":["PhD"]},{"key":"thesis:institution_name","label":"Thesis Institution Name","values":["The University of Texas Medical Branch"]}]},{"id":"subjects_keywords","label":"Subjects and Keywords","entries":[{"key":"dc:subject","label":"Dc Subject","values":["lethal toxin","edema toxin","bacillus anthracis","B cell","anthrax toxin","anthrax"]}]},{"id":"language_rights","label":"Language and Rights","entries":[{"key":"dc:language.iso","label":"Language (ISO)","values":["eng"]},{"key":"dc:rights","label":"Dc Rights","values":["Copyright © is held by the author. Presentation of this material on the TDL web site by The University of Texas Medical Branch at Galveston was made possible under a limited license grant from the author who has retained all copyrights in the works."]}]},{"id":"identifiers","label":"Identifiers","entries":[{"key":"dc:identifier.other","label":"Dc Identifier Other","values":["etd-03112010-180727"]},{"key":"dc:identifier.uri","label":"Identifier URI","values":["http://hdl.handle.net/2152.3/40"]}]},{"id":"additional","label":"Additional Metadata","entries":[{"key":"dc:description.abstract","label":"Abstract","values":["Bacillus anthracis is a gram-positive spore-forming rod capable of causing cutaneous, gastrointestinal and inhalational anthrax. It has a number of virulence factors of which, the two toxins are of great importance. Lethal toxin is a zinc metaloprotease that cleaves the N terminus of the mitogen-activated protein kinase (MAPK) kinase family 1-7, with the exception of MEK5. This kinase family is responsible for activating the mitogen-activated protein kinase (MAPK) cascade. This cascade includes extracellular signal-regulated protein kinases (ERK), c-Jun NH2-terminal kinases (JNK) and p38 kinases. The disruption of these signaling pathways has a number of deleterious downstream effects that vary by cell type. Edema factor is a powerful calmodulin-dependent adenylyl cyclase that forms 3’,5’-adenosine monophosphate (cAMP) from adenosine triphosphate (ATP). This enzymatic reaction causes an increase in intracellular cyclic AMP (cAMP) in host cells. As cAMP is a prominent second messenger in cellular signaling, edema toxin has a wide array of effects on numerous cell types and functions. \\r\\nTo determine the effects of the anthrax toxins on the adaptive immune response, B lymphocytes were exposed to LeTx or EdTx in vitro. LeTx and EdTx both inhibit B cell activation in different manners. LeTx inhibited B cell proliferation but not migration, while EdTx inhibited B cell migration but not proliferation. LeTx and EdTx altered expression patterns of B cell activation markers. EdTx inhibited MIP-1α and MIP-1β while enhancing IL-6 production. Previously unseen in any cell type EdTx was demonstrated to be cytotoxic to naïve B cells.\\r\\nThe research presented in this report illustrates the inhibitory effects of LeTx and EdTx on B lymphocytes, providing valuable insight into the immunoevasion tactics of B. anthracis.\\r\\n"]},{"key":"dc:format.medium","label":"Dc Format Medium","values":["electronic"]},{"key":"dc:title","label":"Title","values":["Anthrax toxin effects on B lymphocyte function"]}]}],"canonical_facts":{"dc:contributor.advisor":["Johnny Peterson"],"dc:contributor.committeemember":["Rolf Konig","Gustavo Valbuena","David Craft"],"dc:creator":["Bryan Thomas Gnade"],"dc:date.accessioned":["2011-12-20T16:04:17Z"],"dc:date.available":["2010-09-28","2011-12-20T16:04:17Z"],"dc:date.issued":["2010-01-11"],"dc:description.abstract":["Bacillus anthracis is a gram-positive spore-forming rod capable of causing cutaneous, gastrointestinal and inhalational anthrax. It has a number of virulence factors of which, the two toxins are of great importance. Lethal toxin is a zinc metaloprotease that cleaves the N terminus of the mitogen-activated protein kinase (MAPK) kinase family 1-7, with the exception of MEK5. This kinase family is responsible for activating the mitogen-activated protein kinase (MAPK) cascade. This cascade includes extracellular signal-regulated protein kinases (ERK), c-Jun NH2-terminal kinases (JNK) and p38 kinases. The disruption of these signaling pathways has a number of deleterious downstream effects that vary by cell type. Edema factor is a powerful calmodulin-dependent adenylyl cyclase that forms 3’,5’-adenosine monophosphate (cAMP) from adenosine triphosphate (ATP). This enzymatic reaction causes an increase in intracellular cyclic AMP (cAMP) in host cells. As cAMP is a prominent second messenger in cellular signaling, edema toxin has a wide array of effects on numerous cell types and functions. \\r\\nTo determine the effects of the anthrax toxins on the adaptive immune response, B lymphocytes were exposed to LeTx or EdTx in vitro. LeTx and EdTx both inhibit B cell activation in different manners. LeTx inhibited B cell proliferation but not migration, while EdTx inhibited B cell migration but not proliferation. LeTx and EdTx altered expression patterns of B cell activation markers. EdTx inhibited MIP-1α and MIP-1β while enhancing IL-6 production. Previously unseen in any cell type EdTx was demonstrated to be cytotoxic to naïve B cells.\\r\\nThe research presented in this report illustrates the inhibitory effects of LeTx and EdTx on B lymphocytes, providing valuable insight into the immunoevasion tactics of B. anthracis.\\r\\n"],"dc:format.medium":["electronic"],"dc:identifier.other":["etd-03112010-180727"],"dc:identifier.uri":["http://hdl.handle.net/2152.3/40"],"dc:language.iso":["eng"],"dc:rights":["Copyright © is held by the author. Presentation of this material on the TDL web site by The University of Texas Medical Branch at Galveston was made possible under a limited license grant from the author who has retained all copyrights in the works."],"dc:subject":["lethal toxin","edema toxin","bacillus anthracis","B cell","anthrax toxin","anthrax"],"dc:title":["Anthrax toxin effects on B lymphocyte function"],"thesis:degree_level":["Doctoral"],"thesis:degree_name":["PhD"],"thesis:institution_name":["The University of Texas Medical Branch"]},"updated_at":"2026-07-24T05:51:10Z"}