{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,10]],"date-time":"2026-09-10T23:30:09Z","timestamp":1789083009924,"version":"build-2803163510"},"reference-count":61,"publisher":"American Society for Microbiology","issue":"1","license":[{"start":{"date-parts":[[2026,1,20]],"date-time":"2026-01-20T00:00:00Z","timestamp":1768867200000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"},{"start":{"date-parts":[[2026,1,20]],"date-time":"2026-01-20T00:00:00Z","timestamp":1768867200000},"content-version":"tdm","delay-in-days":0,"URL":"https:\/\/journals.asm.org\/non-commercial-tdm-license"}],"funder":[{"DOI":"10.13039\/501100004479","name":"Natural Science Foundation of Jiangxi Province","doi-asserted-by":"crossref","award":["20252BAC200441, YFYPY202413, GJJ2400132"],"award-info":[{"award-number":["20252BAC200441, YFYPY202413, GJJ2400132"]}],"id":[{"id":"10.13039\/501100004479","id-type":"DOI","asserted-by":"crossref"}]},{"DOI":"10.13039\/501100004479","name":"Natural Science Foundation of Jiangxi Province","doi-asserted-by":"crossref","award":["20212BAB216041"],"award-info":[{"award-number":["20212BAB216041"]}],"id":[{"id":"10.13039\/501100004479","id-type":"DOI","asserted-by":"crossref"}]},{"DOI":"10.13039\/501100001809","name":"National Natural Science Foundation of China","doi-asserted-by":"crossref","award":["82460397, 82260085"],"award-info":[{"award-number":["82460397, 82260085"]}],"id":[{"id":"10.13039\/501100001809","id-type":"DOI","asserted-by":"crossref"}]}],"content-domain":{"domain":["journals.asm.org"],"crossmark-restriction":true},"short-container-title":["mSystems"],"published-print":{"date-parts":[[2026,1,20]]},"abstract":"<jats:title>ABSTRACT<\/jats:title>\n                  <jats:sec>\n                    <jats:title\/>\n                    <jats:p>\n                      <jats:italic toggle=\"yes\">Pseudomonas aeruginosa<\/jats:italic>\n                      is a predominant colonizer of airways in non-cystic fibrosis bronchiectasis (NCFB), yet its adaptive mechanisms remain poorly understood. This study investigates the genetic characteristics, virulence variation, and resistance mechanisms of 66\n                      <jats:italic toggle=\"yes\">P<\/jats:italic>\n                      .\n                      <jats:italic toggle=\"yes\">aeruginosa<\/jats:italic>\n                      isolates derived from NCFB patients. Whole-genome sequencing revealed extensive genetic diversity, encompassing 53 sequence types and a predominance of the O6 serotype (30\/66, 45.5%). Phylogenetic analysis indicated that most NCFB isolates were acquired independently, with limited evidence of transmission. Extensive loss-of-function mutations were identified, with\n                      <jats:italic toggle=\"yes\">mucA<\/jats:italic>\n                      mutations present in 90.6% (29\/32) of mucoid and 67.6% (23\/34) of non-mucoid isolates. Most\n                      <jats:italic toggle=\"yes\">mucA<\/jats:italic>\n                      mutations were frameshift variants, predominantly at codon 144 (Ala144fs), indicating the selective advantage of this site in driving alginate overproduction during chronic airway infection. Virulence gene profiling demonstrated a highly conserved core repertoire but considerable variability in type VI secretion and pyoverdine systems. Notably, mucoid isolates exhibited significantly higher cefiderocol MICs compared to non-mucoid isolates (\n                      <jats:italic toggle=\"yes\">P<\/jats:italic>\n                      = 0.0073), along with enhanced biofilm formation (\n                      <jats:italic toggle=\"yes\">P<\/jats:italic>\n                      &lt; 0.0001) but reduced virulence in the\n                      <jats:italic toggle=\"yes\">Galleria mellonella<\/jats:italic>\n                      infection model. Mechanistic studies revealed that cefiderocol resistance in mucoid\n                      <jats:italic toggle=\"yes\">P. aeruginosa<\/jats:italic>\n                      was driven by synergistic interactions between alginate overproduction and mutations in iron-uptake regulatory genes, particularly Gly132 frameshift in\n                      <jats:italic toggle=\"yes\">pirR<\/jats:italic>\n                      . Disruption of alginate biosynthesis (\u0394\n                      <jats:italic toggle=\"yes\">algD<\/jats:italic>\n                      ) and complementation of\n                      <jats:italic toggle=\"yes\">pirR<\/jats:italic>\n                      in mucoid strains markedly restored cefiderocol susceptibility. These findings highlight the remarkable genomic diversity and adaptive resistance mechanisms of\n                      <jats:italic toggle=\"yes\">P. aeruginosa<\/jats:italic>\n                      in NCFB, providing important insights into its persistence and therapeutic challenges in chronic airway infection.\n                    <\/jats:p>\n                    <jats:sec>\n                      <jats:title>IMPORTANCE<\/jats:title>\n                      <jats:p>\n                        Understanding the adaptive mechanisms of\n                        <jats:italic toggle=\"yes\">Pseudomonas aeruginosa<\/jats:italic>\n                        in non-cystic fibrosis bronchiectasis (NCFB) is critical for improving treatment strategies. This study reveals substantial genomic diversity and highlights alginate overproduction as a key feature of chronic adaptation. Notably, we uncover a novel resistance mechanism involving synergistic interactions between alginate production and mutations in iron-uptake regulators, particularly\n                        <jats:italic toggle=\"yes\">pirR<\/jats:italic>\n                        . These findings underscore the complex evolutionary pressures shaping\n                        <jats:italic toggle=\"yes\">P. aeruginosa<\/jats:italic>\n                        persistence in NCFB and provide valuable insights into its resistance and virulence balance, offering potential targets for more effective therapeutic interventions.\n                      <\/jats:p>\n                    <\/jats:sec>\n                  <\/jats:sec>","DOI":"10.1128\/msystems.01514-25","type":"journal-article","created":{"date-parts":[[2025,12,5]],"date-time":"2025-12-05T14:01:10Z","timestamp":1764943270000},"update-policy":"https:\/\/doi.org\/10.1128\/asmj-crossmark-policy-page","source":"Crossref","is-referenced-by-count":3,"title":["Genomic diversity and adaptive resistance mechanisms in\n                    <i>Pseudomonas aeruginosa<\/i>\n                    from bronchiectasis"],"prefix":"10.1128","volume":"11","author":[{"ORCID":"https:\/\/orcid.org\/0000-0001-7417-0799","authenticated-orcid":false,"given":"Yanghua","family":"Xiao","sequence":"first","affiliation":[{"id":[{"id":"https:\/\/ror.org\/042v6xz23","id-type":"ROR","asserted-by":"publisher"}],"name":"Department of Respiratory and Critical Care Medicine, The First Affiliated Hospital, Jiangxi Medical College, Nanchang University","place":["Nanchang, China"]},{"id":[{"id":"https:\/\/ror.org\/042v6xz23","id-type":"ROR","asserted-by":"publisher"}],"name":"Jiangxi Provincial Key Laboratory of Respiratory Diseases, Jiangxi Institute of Respiratory Diseases, The First Affiliated Hospital, Jiangxi Medical College, Nanchang University","place":["Nanchang, 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