{"id":{"repo_id":"goteborg","oai_identifier":"oai:gupea.ub.gu.se:2077/52858"},"canonical_url":"https://search.dev.ndltd.org/etd/goteborg/oai:gupea.ub.gu.se:2077/52858","repository":{"repo_id":"goteborg","name":"Gothenburg University","base_url":"https://gupea.ub.gu.se/oai/request"},"display":{"title":"The IL-23 axis and innate immunity in the airways","abstract":"The Interleukin-23 (IL-23) axis is a communication system that integrates innate and adaptive immunity. When triggered by microbial stimuli, antigen presenting cells can secrete the cytokine IL-23, leading to the production of IL-17 and IL-22. These cytokines facilitate the recruitment of neutrophils that can eliminate microbes, but may also cause epithelial damage through extensive inflammation. At the same time, the IL-23 axis protects the epithelium through the production of antimicrobial peptides. The protective role of the IL-23 axis for local epithelial defence led us to ask whether inflammatory cells of the airway epithelium can produce IL-22, a cytokine associated with the IL-23 axis. We showed that airway macrophages responded to IL-23 and a bacterial stimulus with the secretion of IL-22. This constitutes a local and accessible source of IL-22 during activation of the innate arm of pulmonary host defence. The IL-23 axis leads to neutrophil recruitment which risks damaging epithelial tissue. Therefore, a strict regulation of the production of these cytokines is necessary. We showed that IL-17 exerts a negative feedback effect on IL-23, thus decreasing its own production. Further, the IL-17 receptor was present on macrophages demonstrating a prerequisite to this response. The airway epithelium is protected by antimicrobial peptides functioning as innate antibiotics, several of which are regulated by the IL-23 axis. We demonstrated the expression of two antimicrobial peptides, calprotectin and LL-37, in healthy human airways. Of these, only LL-37 was induced by the gram-negative bacterial stimulus endotoxin in this setting. This demonstrates the involvement of LL-37 in the innate immune response against gramnegative bacteria. Finally, we quantified cytokines associated with the IL-23 axis in smokers with and without chronic obstructive pulmonary disease. Airway IL-17 did not differ significantly between the groups, but plasma IL-22 was increased in smokers, demonstrating a smoking induced systemic effect on the IL-23 axis. Neutrophils in the airways displayed signs of activation and could be further activated by TNFα, indicating that the local microenvironment can affect neutrophil activation.","abstract_html":"The Interleukin-23 (IL-23) axis is a communication system that integrates innate and adaptive immunity. When triggered by microbial stimuli, antigen presenting cells can secrete the cytokine IL-23, leading to the production of IL-17 and IL-22. These cytokines facilitate the recruitment of neutrophils that can eliminate microbes, but may also cause epithelial damage through extensive inflammation. At the same time, the IL-23 axis protects the epithelium through the production of antimicrobial peptides. The protective role of the IL-23 axis for local epithelial defence led us to ask whether inflammatory cells of the airway epithelium can produce IL-22, a cytokine associated with the IL-23 axis. We showed that airway macrophages responded to IL-23 and a bacterial stimulus with the secretion of IL-22. This constitutes a local and accessible source of IL-22 during activation of the innate arm of pulmonary host defence. The IL-23 axis leads to neutrophil recruitment which risks damaging epithelial tissue. Therefore, a strict regulation of the production of these cytokines is necessary. We showed that IL-17 exerts a negative feedback effect on IL-23, thus decreasing its own production. Further, the IL-17 receptor was present on macrophages demonstrating a prerequisite to this response. The airway epithelium is protected by antimicrobial peptides functioning as innate antibiotics, several of which are regulated by the IL-23 axis. We demonstrated the expression of two antimicrobial peptides, calprotectin and LL-37, in healthy human airways. Of these, only LL-37 was induced by the gram-negative bacterial stimulus endotoxin in this setting. This demonstrates the involvement of LL-37 in the innate immune response against gramnegative bacteria. Finally, we quantified cytokines associated with the IL-23 axis in smokers with and without chronic obstructive pulmonary disease. Airway IL-17 did not differ significantly between the groups, but plasma IL-22 was increased in smokers, demonstrating a smoking induced systemic effect on the IL-23 axis. Neutrophils in the airways displayed signs of activation and could be further activated by TNFα, indicating that the local microenvironment can affect neutrophil activation.","abstract_has_math":false,"creators":["Stockfelt, Marit"],"institution":null,"degree_name":null,"degree_level":null,"degree_discipline":null,"degree_department":null,"school":null,"contributors":[],"advisors":[],"committee_chairs":[],"committee_members":[],"year":2017,"date_issued":"2017-11-08","date_published":"2017-11-08","updated_at":"2026-08-21T22:21:56Z","subjects":["IL-23","airways"],"languages":["eng"],"rights":[],"rights_urls":[],"identifier_entries":[]},"links":{"outbound_url":"http://hdl.handle.net/2077/52858","outbound_label":"Handle","outbound_source":"dc:identifier.uri"},"source_record":{"url":"https://gupea.ub.gu.se/oai/request?verb=GetRecord&metadataPrefix=dim&identifier=oai%3Agupea.ub.gu.se%3A2077%2F52858","prefix":"dim"},"metadata_groups":[{"id":"people","label":"People","entries":[{"key":"dc:creator","label":"Author","values":["Stockfelt, Marit"]}]},{"id":"academic_context","label":"Academic Context","entries":[{"key":"dc:date.accessioned","label":"Dc Date Accessioned","values":["2017-11-08T15:11:31Z"]},{"key":"dc:date.available","label":"Dc Date Available","values":["2017-11-08T15:11:31Z"]},{"key":"dc:date.issued","label":"Date","values":["2017-11-08"]},{"key":"dc:type","label":"Dc Type","values":["text"]}]},{"id":"subjects_keywords","label":"Subjects and Keywords","entries":[{"key":"dc:subject","label":"Dc Subject","values":["IL-23","airways"]}]},{"id":"language_rights","label":"Language and Rights","entries":[{"key":"dc:language.iso","label":"Language (ISO)","values":["eng"]}]},{"id":"identifiers","label":"Identifiers","entries":[{"key":"dc:identifier.uri","label":"Identifier URI","values":["http://hdl.handle.net/2077/52858"]}]},{"id":"additional","label":"Additional Metadata","entries":[{"key":"dc:description.abstract","label":"Abstract","values":["The Interleukin-23 (IL-23) axis is a communication system that integrates innate and adaptive immunity. When triggered by microbial stimuli, antigen presenting cells can secrete the cytokine IL-23, leading to the production of IL-17 and IL-22. These cytokines facilitate the recruitment of neutrophils that can eliminate microbes, but may also cause epithelial damage through extensive inflammation. At the same time, the IL-23 axis protects the epithelium through the production of antimicrobial peptides. The protective role of the IL-23 axis for local epithelial defence led us to ask whether inflammatory cells of the airway epithelium can produce IL-22, a cytokine associated with the IL-23 axis. We showed that airway macrophages responded to IL-23 and a bacterial stimulus with the secretion of IL-22. This constitutes a local and accessible source of IL-22 during activation of the innate arm of pulmonary host defence. The IL-23 axis leads to neutrophil recruitment which risks damaging epithelial tissue. Therefore, a strict regulation of the production of these cytokines is necessary. We showed that IL-17 exerts a negative feedback effect on IL-23, thus decreasing its own production. Further, the IL-17 receptor was present on macrophages demonstrating a prerequisite to this response. The airway epithelium is protected by antimicrobial peptides functioning as innate antibiotics, several of which are regulated by the IL-23 axis. We demonstrated the expression of two antimicrobial peptides, calprotectin and LL-37, in healthy human airways. Of these, only LL-37 was induced by the gram-negative bacterial stimulus endotoxin in this setting. This demonstrates the involvement of LL-37 in the innate immune response against gramnegative bacteria. Finally, we quantified cytokines associated with the IL-23 axis in smokers with and without chronic obstructive pulmonary disease. Airway IL-17 did not differ significantly between the groups, but plasma IL-22 was increased in smokers, demonstrating a smoking induced systemic effect on the IL-23 axis. Neutrophils in the airways displayed signs of activation and could be further activated by TNFα, indicating that the local microenvironment can affect neutrophil activation."]},{"key":"dc:title","label":"Title","values":["The IL-23 axis and innate immunity in the airways"]}]}],"canonical_facts":{"dc:creator":["Stockfelt, Marit"],"dc:date.accessioned":["2017-11-08T15:11:31Z"],"dc:date.available":["2017-11-08T15:11:31Z"],"dc:date.issued":["2017-11-08"],"dc:description.abstract":["The Interleukin-23 (IL-23) axis is a communication system that integrates innate and adaptive immunity. When triggered by microbial stimuli, antigen presenting cells can secrete the cytokine IL-23, leading to the production of IL-17 and IL-22. These cytokines facilitate the recruitment of neutrophils that can eliminate microbes, but may also cause epithelial damage through extensive inflammation. At the same time, the IL-23 axis protects the epithelium through the production of antimicrobial peptides. The protective role of the IL-23 axis for local epithelial defence led us to ask whether inflammatory cells of the airway epithelium can produce IL-22, a cytokine associated with the IL-23 axis. We showed that airway macrophages responded to IL-23 and a bacterial stimulus with the secretion of IL-22. This constitutes a local and accessible source of IL-22 during activation of the innate arm of pulmonary host defence. The IL-23 axis leads to neutrophil recruitment which risks damaging epithelial tissue. Therefore, a strict regulation of the production of these cytokines is necessary. We showed that IL-17 exerts a negative feedback effect on IL-23, thus decreasing its own production. Further, the IL-17 receptor was present on macrophages demonstrating a prerequisite to this response. The airway epithelium is protected by antimicrobial peptides functioning as innate antibiotics, several of which are regulated by the IL-23 axis. We demonstrated the expression of two antimicrobial peptides, calprotectin and LL-37, in healthy human airways. Of these, only LL-37 was induced by the gram-negative bacterial stimulus endotoxin in this setting. This demonstrates the involvement of LL-37 in the innate immune response against gramnegative bacteria. Finally, we quantified cytokines associated with the IL-23 axis in smokers with and without chronic obstructive pulmonary disease. Airway IL-17 did not differ significantly between the groups, but plasma IL-22 was increased in smokers, demonstrating a smoking induced systemic effect on the IL-23 axis. Neutrophils in the airways displayed signs of activation and could be further activated by TNFα, indicating that the local microenvironment can affect neutrophil activation."],"dc:identifier.uri":["http://hdl.handle.net/2077/52858"],"dc:language.iso":["eng"],"dc:subject":["IL-23","airways"],"dc:title":["The IL-23 axis and innate immunity in the airways"],"dc:type":["text"]},"updated_at":"2026-08-21T22:21:56Z"}