{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"institution":[{"name":"bioRxiv"}],"indexed":{"date-parts":[[2026,10,31]],"date-time":"2026-10-31T11:34:18Z","timestamp":1793446458202,"version":"4.5.0"},"posted":{"date-parts":[[2026,9,20]]},"group-title":"Immunology","reference-count":124,"publisher":"openRxiv","license":[{"start":{"date-parts":[[2026,9,20]],"date-time":"2026-09-20T00:00:00Z","timestamp":1789862400000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/www.biorxiv.org\/about\/FAQ#license"}],"funder":[{"award":["T32HL134598"],"award-info":[{"award-number":["T32HL134598"]}],"id":[{"id":"https:\/\/ror.org\/01cwqze88","id-type":"ROR","asserted-by":"publisher"}]},{"name":"Cystic Fibrosis Foundation","award":["BLISKA24I0"],"award-info":[{"award-number":["BLISKA24I0"]}],"id":[{"id":"https:\/\/ror.org\/00ax59295","id-type":"ROR","asserted-by":"crossref"}]},{"name":"The Philip Hanlon and Gail Gentes Cluster for Personalized Treatments for Cystic Fibrosis"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"accepted":{"date-parts":[[2026,10,28]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                <jats:p>\n                  <jats:italic>Pseudomonas aeruginosa<\/jats:italic>\n                  is an important agent of acute or chronic airway infections. A complex set of genetic and environmental factors determine outcomes of\n                  <jats:italic>P. aeruginosa<\/jats:italic>\n                  airway infections.\n                <\/jats:p>\n                <jats:p>\n                  <jats:italic>P. aeruginosa<\/jats:italic>\n                  undergoes genetic adaptation to finetune expression of a type III secretion system (T3SS) and other virulence factors in response to selective pressures during infection. Genetic and environmental factors predispose for\n                  <jats:italic>P. aeruginosa<\/jats:italic>\n                  infections in patients such as those with cystic fibrosis (CF). CF is a genetic disorder resulting in hypoxia and thick mucus that fosters\n                  <jats:italic>P. aeruginosa<\/jats:italic>\n                  airway infection. Resident alveolar macrophages (AMs) coordinate immune responses to\n                  <jats:italic>P. aeruginosa<\/jats:italic>\n                  by producing proinflammatory cytokines such as IL-1\u03b2, which can promote infection resistance. AMs infected with\n                  <jats:italic>P. aeruginosa<\/jats:italic>\n                  laboratory strains detect the T3SS and activate the NLRC4 inflammasome, resulting in IL-1\u03b2 release. Studies of inflammasome responses in AMs to a\n                  <jats:italic>P. aeruginosa<\/jats:italic>\n                  CF isolate of have not been reported. Here, we characterized the CF isolate DH1137 and found it has a downregulated but functional T3SS, is adapted to grow in hypoxia, and induces significant production of the inflammasome cytokines IL-1\u03b1 and IL-1\u03b2 during acute lung infection in a CF mouse model. Inflammasome gene expression was primed in AMs by LPS, and upon DH1137 infection these cells released IL-1\u03b2. Infection of AMs with DH1137 or laboratory strain PAO1 in hypoxia resulted in significantly dampened inflammasome activation compared to normoxia. These data describe a new mechanism that\n                  <jats:italic>P. aeruginosa<\/jats:italic>\n                  may exploit to evade immune detection by tissue-resident lung macrophages in the context of CF.\n                <\/jats:p>\n                <jats:sec>\n                  <jats:title>Importance<\/jats:title>\n                  <jats:p>\n                    Airway infection of people with CF by\n                    <jats:italic>P. aeruginosa<\/jats:italic>\n                    results from genetic and environmental changes that impact host and pathogen. Mutations in the cystic fibrosis transmembrane conductance regulator gene (\n                    <jats:italic>CFTR<\/jats:italic>\n                    ) cause anatomical alterations in airways, including areas of hypoxia, that compromise anti-bacterial defense.\n                    <jats:italic>P. aeruginosa<\/jats:italic>\n                    genetically adapts by downregulating a T3SS important for establishment and turning up phenotypes that promote chronic infection such as hypoxic growth. AMs are resident airway phagocytes that can normally detect\n                    <jats:italic>P. aeruginosa and<\/jats:italic>\n                    undergo inflammasome activation to release IL-1 cytokines, however these cells are known to be dysregulated in CF, and their interactions with clinical isolates are understudied. Here show that\n                    <jats:italic>P. aeruginosa<\/jats:italic>\n                    elicits IL-1 cytokines during acute lung infection in a CF mouse model but triggers low inflammasome activation in hypoxic AMs ex vivo, suggesting the bacterium exploits low oxygen to evade detection by resident lung macrophages in CF.\n                  <\/jats:p>\n                <\/jats:sec>","DOI":"10.64898\/2026.09.14.750667","type":"posted-content","created":{"date-parts":[[2026,9,21]],"date-time":"2026-09-21T04:00:13Z","timestamp":1789963213000},"source":"Crossref","is-referenced-by-count":1,"title":["Inflammasome Activation and IL-1\u03b2 Release in Alveolar Macrophages Infected with\n                  <i>Pseudomonas aeruginosa<\/i>\n                  is Reduced in Hypoxia"],"prefix":"10.64898","author":[{"given":"Alexander W.","family":"Rapp","sequence":"first","affiliation":[{"name":"Department of Microbiology & Immunology, Geisel School of Medicine at Dartmouth, Hanover, NH 03755, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Aurora L.","family":"Golden","sequence":"additional","affiliation":[{"name":"Department of Microbiology & Immunology, Geisel School of Medicine at Dartmouth, Hanover, NH 03755, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Arianna D.","family":"Reuven","sequence":"additional","affiliation":[{"name":"Department of Microbiology & Immunology, Geisel School of Medicine at Dartmouth, Hanover, NH 03755, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jay","family":"Goddard","sequence":"additional","affiliation":[{"name":"Department of Microbiology & Immunology, Geisel School of Medicine at Dartmouth, Hanover, NH 03755, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Emily Ann","family":"McClure","sequence":"additional","affiliation":[{"name":"Department of Microbiology & Immunology, Geisel School of Medicine at Dartmouth, Hanover, NH 03755, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Aimee M.","family":"Wilson","sequence":"additional","affiliation":[{"name":"Department of Microbiology & Immunology, Geisel School of Medicine at Dartmouth, Hanover, NH 03755, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Chloe A.","family":"Young","sequence":"additional","affiliation":[{"name":"Department of Microbiology & Immunology, Geisel School of Medicine at Dartmouth, Hanover, NH 03755, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Caitlin E.","family":"Murphy","sequence":"additional","affiliation":[{"name":"Department of Microbiology & Immunology, Geisel School of Medicine at Dartmouth, Hanover, NH 03755, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Taalia-Lindsay","family":"Morgan","sequence":"additional","affiliation":[{"name":"Department of Microbiology & Immunology, Geisel School of Medicine at Dartmouth, Hanover, NH 03755, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Andrew J.","family":"Olive","sequence":"additional","affiliation":[{"name":"Department of Microbiology & Molecular Genetics, College of Osteopathic Medicine, Michigan State University, East Lansing, MI 48824, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-4068-7911","authenticated-orcid":false,"given":"Joshua J.","family":"Obar","sequence":"additional","affiliation":[{"name":"Department of Microbiology & Immunology, Geisel School of Medicine at Dartmouth, Hanover, NH 03755, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Deborah A.","family":"Hogan","sequence":"additional","affiliation":[{"name":"Department of Microbiology & Immunology, Geisel School of Medicine at Dartmouth, Hanover, NH 03755, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-8817-3138","authenticated-orcid":false,"given":"Benjamin D.","family":"Ross","sequence":"additional","affiliation":[{"name":"Department of Microbiology & Immunology, Geisel School of Medicine at Dartmouth, Hanover, NH 03755, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-6047-8837","authenticated-orcid":false,"given":"James B.","family":"Bliska","sequence":"additional","affiliation":[{"name":"Department of Microbiology & Immunology, Geisel School of Medicine at Dartmouth, Hanover, NH 03755, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"54368","reference":[{"key":"2026103104251038000_2026.09.14.750667v2.1","doi-asserted-by":"publisher","DOI":"10.3390\/ijms22063128"},{"key":"2026103104251038000_2026.09.14.750667v2.2","doi-asserted-by":"publisher","DOI":"10.1016\/j.micinf.2011.07.011"},{"key":"2026103104251038000_2026.09.14.750667v2.3","doi-asserted-by":"publisher","DOI":"10.1159\/000455857"},{"key":"2026103104251038000_2026.09.14.750667v2.4","unstructured":"Reuven AD , Bliska JB. 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