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People with CF (pwCF) are often colonized with\n                      <jats:italic toggle=\"yes\">Pseudomonas aeruginosa<\/jats:italic>\n                      for years to decades, allowing for evolutionary adaptation. In chronic\n                      <jats:italic toggle=\"yes\">P. aeruginosa<\/jats:italic>\n                      lung isolates from pwCF, the quorum-sensing regulator LasR is frequently nonfunctional; however, the factors enabling\n                      <jats:italic toggle=\"yes\">lasR<\/jats:italic>\n                      loss-of-function (LOF) mutant selection are incompletely understood. We hypothesized that LOF mutations in\n                      <jats:italic toggle=\"yes\">lasR<\/jats:italic>\n                      could allow\n                      <jats:italic toggle=\"yes\">P. aeruginosa<\/jats:italic>\n                      to resist the selective pressure of phagocytosis. We found that in multiple strain backgrounds, LasR LOF decreased phagocytosis by both model THP-1 and primary monocyte-derived macrophages, and\n                      <jats:italic toggle=\"yes\">lasR<\/jats:italic>\n                      complementation increased phagocytosis in mutant strains. While exogenous administration of the quorum-sensing autoinducer 3-oxo-C12-homoserine-lactone, which is made by an enzyme regulated by LasR activity, inhibited phagocytosis and mitochondrial respiration, the phagocytosis resistance seen with\n                      <jats:italic toggle=\"yes\">lasR<\/jats:italic>\n                      mutants appears to be bacterial cell intrinsic rather than due to secreted factors. Finally, we found that\n                      <jats:italic toggle=\"yes\">lasR<\/jats:italic>\n                      LOF mutations altered the inflammatory profile upon infection of CF macrophages, with a shift from IL-1 family cytokine expression toward canonical inflammatory markers, including IL-6 and TNF\u03b1. Collectively, these data provide a potential explanation for both the prevalence of\n                      <jats:italic toggle=\"yes\">lasR<\/jats:italic>\n                      mutants in the CF lung as well as their association with worse outcomes.\n                    <\/jats:p>\n                    <jats:sec>\n                      <jats:title>IMPORTANCE<\/jats:title>\n                      <jats:p>\n                        Cystic fibrosis (CF) is a genetically inherited disease that leads to chronic lung infections.\n                        <jats:italic toggle=\"yes\">Pseudomonas aeruginosa<\/jats:italic>\n                        is often implicated in the worsening of lung disease, and it evolves in the lung over time to resist eradication. One of the most commonly disrupted genes in\n                        <jats:italic toggle=\"yes\">P. aeruginosa<\/jats:italic>\n                        isolates from chronically infected CF lungs is\n                        <jats:italic toggle=\"yes\">lasR<\/jats:italic>\n                        , which encodes a transcription factor that regulates multiple virulence factors. What contributes to the apparent fitness of\n                        <jats:italic toggle=\"yes\">lasR<\/jats:italic>\n                        mutants in the CF lung is not well known. Our study shows that\n                        <jats:italic toggle=\"yes\">lasR<\/jats:italic>\n                        loss-of-function mutants resist phagocytosis by macrophages, one of the fundamental mechanisms of clearance by the immune system. We identify mechanisms promoting resistance to phagocytosis and explore the downstream consequences on inflammatory responses. Understanding why\n                        <jats:italic toggle=\"yes\">lasR<\/jats:italic>\n                        mutations arise could inform strategies to eradicate them from the CF lung and improve outcomes.\n                      <\/jats:p>\n                    <\/jats:sec>\n                  <\/jats:sec>","DOI":"10.1128\/msphere.00702-25","type":"journal-article","created":{"date-parts":[[2026,4,2]],"date-time":"2026-04-02T13:00:17Z","timestamp":1775134817000},"update-policy":"https:\/\/doi.org\/10.1128\/asmj-crossmark-policy-page","source":"Crossref","is-referenced-by-count":1,"title":["<i>Pseudomonas aeruginosa lasR<\/i>\n                    mutants resist phagocytosis and alter inflammatory cytokine production by cystic fibrosis macrophages"],"prefix":"10.1128","volume":"11","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-6132-6472","authenticated-orcid":true,"given":"Daniel S.","family":"Aridgides","sequence":"first","affiliation":[{"id":[{"id":"https:\/\/ror.org\/00d1dhh09","id-type":"ROR","asserted-by":"publisher"}],"name":"Section of Pulmonary and Critical Care Medicine, Dartmouth-Hitchcock Medical Center","place":["Lebanon, USA"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Diane L.","family":"Mellinger","sequence":"additional","affiliation":[{"id":[{"id":"https:\/\/ror.org\/00d1dhh09","id-type":"ROR","asserted-by":"publisher"}],"name":"Section of Pulmonary and Critical Care Medicine, Dartmouth-Hitchcock Medical Center","place":["Lebanon, USA"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Lorraine L.","family":"Gwilt","sequence":"additional","affiliation":[{"id":[{"id":"https:\/\/ror.org\/00d1dhh09","id-type":"ROR","asserted-by":"publisher"}],"name":"Section of Pulmonary and Critical Care Medicine, Dartmouth-Hitchcock Medical Center","place":["Lebanon, USA"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Anthony R.","family":"Correia","sequence":"additional","affiliation":[{"id":[{"id":"https:\/\/ror.org\/00d1dhh09","id-type":"ROR","asserted-by":"publisher"}],"name":"Section of Pulmonary and Critical Care Medicine, Dartmouth-Hitchcock Medical Center","place":["Lebanon, USA"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Carson E.","family":"Finger","sequence":"additional","affiliation":[{"id":[{"id":"https:\/\/ror.org\/00d1dhh09","id-type":"ROR","asserted-by":"publisher"}],"name":"Department of Microbiology and Immunology, Dartmouth Geisel School of Medicine","place":["Hanover, USA"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jay","family":"Goddard","sequence":"additional","affiliation":[{"id":[{"id":"https:\/\/ror.org\/00d1dhh09","id-type":"ROR","asserted-by":"publisher"}],"name":"Department of Microbiology and Immunology, Dartmouth Geisel School of Medicine","place":["Hanover, USA"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-0543-402X","authenticated-orcid":true,"given":"Thomas H.","family":"Hampton","sequence":"additional","affiliation":[{"id":[{"id":"https:\/\/ror.org\/00d1dhh09","id-type":"ROR","asserted-by":"publisher"}],"name":"Department of Microbiology and Immunology, Dartmouth Geisel School of Medicine","place":["Hanover, USA"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Dallas L.","family":"Mould","sequence":"additional","affiliation":[{"id":[{"id":"https:\/\/ror.org\/00d1dhh09","id-type":"ROR","asserted-by":"publisher"}],"name":"Department of Microbiology and Immunology, Dartmouth Geisel School of Medicine","place":["Hanover, USA"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Deborah A.","family":"Hogan","sequence":"additional","affiliation":[{"id":[{"id":"https:\/\/ror.org\/00d1dhh09","id-type":"ROR","asserted-by":"publisher"}],"name":"Department of Microbiology and Immunology, Dartmouth Geisel School of Medicine","place":["Hanover, USA"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Alix","family":"Ashare","sequence":"additional","affiliation":[{"id":[{"id":"https:\/\/ror.org\/00d1dhh09","id-type":"ROR","asserted-by":"publisher"}],"name":"Section of Pulmonary and Critical Care Medicine, Dartmouth-Hitchcock Medical Center","place":["Lebanon, USA"]},{"id":[{"id":"https:\/\/ror.org\/00d1dhh09","id-type":"ROR","asserted-by":"publisher"}],"name":"Department of Microbiology and Immunology, Dartmouth Geisel School of Medicine","place":["Hanover, USA"]}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"235","reference":[{"key":"e_1_3_4_2_2","doi-asserted-by":"publisher","DOI":"10.1016\/S0140-6736(16)00576-6"},{"key":"e_1_3_4_3_2","unstructured":"Cystic Fibrosis Foundation. 2022. 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