{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,9]],"date-time":"2026-09-09T13:11:59Z","timestamp":1788959519089,"version":"build-2803163510"},"reference-count":61,"publisher":"American Society for Microbiology","issue":"9","license":[{"start":{"date-parts":[[2026,9,9]],"date-time":"2026-09-09T00:00:00Z","timestamp":1788912000000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"},{"start":{"date-parts":[[2026,9,9]],"date-time":"2026-09-09T00:00:00Z","timestamp":1788912000000},"content-version":"tdm","delay-in-days":0,"URL":"https:\/\/journals.asm.org\/non-commercial-tdm-license"}],"funder":[{"DOI":"10.13039\/100000002","name":"National Institutes of Health","doi-asserted-by":"publisher","award":["R01AI186380"],"award-info":[{"award-number":["R01AI186380"]}],"id":[{"id":"10.13039\/100000002","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000002","name":"National Institutes of Health","doi-asserted-by":"publisher","award":["R01AI69865"],"award-info":[{"award-number":["R01AI69865"]}],"id":[{"id":"10.13039\/100000002","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000897","name":"Cystic Fibrosis Foundation","doi-asserted-by":"publisher","award":["McCoy24"],"award-info":[{"award-number":["McCoy24"]}],"id":[{"id":"10.13039\/100000897","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000002","name":"National Institutes of Health","doi-asserted-by":"publisher","award":["CCSG P30CA016058"],"award-info":[{"award-number":["CCSG P30CA016058"]}],"id":[{"id":"10.13039\/100000002","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["journals.asm.org"],"crossmark-restriction":true},"short-container-title":["mBio"],"published-print":{"date-parts":[[2026,9,9]]},"abstract":"<jats:title>ABSTRACT<\/jats:title>\n                  <jats:sec>\n                    <jats:title\/>\n                    <jats:p>\n                      In chronic, recalcitrant infections,\n                      <jats:italic toggle=\"yes\">Pseudomonas aeruginosa<\/jats:italic>\n                      forms biofilm aggregates that are encapsulated in a protective extracellular matrix made of exopolysaccharides, extracellular DNA, and matrix proteins. Biofilm formation is a major cause of antibiotic clearance failure in\n                      <jats:italic toggle=\"yes\">P. aeruginosa<\/jats:italic>\n                      , and there is growing pressure to elucidate biofilm preventative measures and develop novel anti-biofilm treatments. Toward this goal, much work has been done to understand the genetic adaptations\n                      <jats:italic toggle=\"yes\">P. aeruginosa<\/jats:italic>\n                      undergoes in chronic respiratory infections, but how the mucosal environment, found in the lung, impacts\n                      <jats:italic toggle=\"yes\">P. aeruginosa<\/jats:italic>\n                      behavior is unclear. Mucus is a protective hydrogel lining wet epithelial cells and is mainly composed of water and its structural component, the glycoprotein mucin. Using commercially purified porcine gastric mucin, which is missing its end tail regions and has modified glycosylation, as a model of structurally altered mucus, we show that\n                      <jats:italic toggle=\"yes\">P. aeruginosa<\/jats:italic>\n                      rapidly increases surface exploration via twitching motility, depositing trails of the exopolysaccharide Psl and elevating total Psl levels. This increased Psl production occurs on short timescales (&lt;1 h), is independent of transcriptional or translational regulation, and enhances tolerance to select antimicrobials, including hydrogen peroxide and ciprofloxacin. Together, these findings indicate that structurally altered mucus environments function as contextual signals that elicit rapid, non-genetic bacterial adaptive behaviors relevant to persistence in chronic infection.\n                    <\/jats:p>\n                    <jats:sec>\n                      <jats:title>IMPORTANCE<\/jats:title>\n                      <jats:p>\n                        Understanding how the host environment impacts pathogen behavior is crucial for developing effective treatments for infections. Here, we provide evidence that the mucosal glycoprotein, mucin, and the O-glycans that decorate the mucin protein backbone alter surface exploration by stimulating twitching motility in the opportunistic pathogen\n                        <jats:italic toggle=\"yes\">Pseudomonas aeruginosa<\/jats:italic>\n                        . This increase in twitching then results in an extensive network of Psl trails, which are a precursor to microcolony formation. Mucin additionally promotes Psl production in a novel post-translational manner across a small cohort of isolates, suggesting Psl production by mucin is conserved. This increase in Psl production was found to also protect cells from killing by antimicrobials. Independent of mucin, we present evidence that the secondary messenger, c-di-GMP, can also post-translationally regulate Psl production, which is the first evidence of post-translational regulation for this exopolysaccharide.\n                      <\/jats:p>\n                    <\/jats:sec>\n                  <\/jats:sec>","DOI":"10.1128\/mbio.01445-26","type":"journal-article","created":{"date-parts":[[2026,8,13]],"date-time":"2026-08-13T13:00:16Z","timestamp":1786626016000},"update-policy":"https:\/\/doi.org\/10.1128\/asmj-crossmark-policy-page","source":"Crossref","is-referenced-by-count":0,"title":["Mucin promotes Psl production and surface exploration in\n                    <i>Pseudomonas aeruginosa<\/i>"],"prefix":"10.1128","volume":"17","author":[{"ORCID":"https:\/\/orcid.org\/0000-0001-8954-7683","authenticated-orcid":false,"given":"Sabrina I.","family":"Lamont","sequence":"first","affiliation":[{"name":"Department of Microbiology, Ohio State University","place":["Columbus, USA"]},{"name":"Department of Microbial Infection and Immunity, Ohio State University College of Medicine","place":["Columbus, USA"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-7609-7537","authenticated-orcid":true,"given":"Matthew J.","family":"Pestrak","sequence":"additional","affiliation":[{"name":"Department of Microbial Infection and Immunity, Ohio State University College of Medicine","place":["Columbus, USA"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Matthew R.","family":"Parsek","sequence":"additional","affiliation":[{"id":[{"id":"https:\/\/ror.org\/00cvxb145","id-type":"ROR","asserted-by":"publisher"}],"name":"Department of Microbiology, University of Washington School of Medicine","place":["Seattle, 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