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These infections involve complex interactions between\n                      <jats:italic toggle=\"yes\">P. aeruginosa<\/jats:italic>\n                      and the airway mucosal epithelium, which are regulated by multiple factors including bacterial adhesion. Calcium (Ca\n                      <jats:sup>2+<\/jats:sup>\n                      ), a potent cellular signal, the levels of which increase in the airway fluids during CF, was shown to alter the expression of multiple virulence factors in\n                      <jats:italic toggle=\"yes\">P. aeruginosa<\/jats:italic>\n                      . However, its role in regulating the host-pathogen interactions is not well understood. This study investigates the impact of Ca\n                      <jats:sup>2+<\/jats:sup>\n                      on the initial adherence of\n                      <jats:italic toggle=\"yes\">P. aeruginosa<\/jats:italic>\n                      to lung epithelial cells and its role in regulating the expression of several adhesins, including flagellin (\n                      <jats:italic toggle=\"yes\">fliC<\/jats:italic>\n                      ), type IV fimbrial precursor (\n                      <jats:italic toggle=\"yes\">pilA<\/jats:italic>\n                      ), and galactophilic lectin (\n                      <jats:italic toggle=\"yes\">lecA<\/jats:italic>\n                      ). Two epithelial cell lines, A549 and CuFi-5 cells, were infected with two strains of\n                      <jats:italic toggle=\"yes\">P. aeruginosa<\/jats:italic>\n                      , PAO1 and FRD1. According to quantitative adherence assays, immunofluorescence microscopy, and scanning electron microscopy, adherence of\n                      <jats:italic toggle=\"yes\">P. aeruginosa<\/jats:italic>\n                      to both cell lines was enhanced at elevated Ca\n                      <jats:sup>2+<\/jats:sup>\n                      . RNA-seq and RT-qPCR showed the transcription of adhesins (\n                      <jats:italic toggle=\"yes\">fliC, pilA,<\/jats:italic>\n                      and\n                      <jats:italic toggle=\"yes\">lecA<\/jats:italic>\n                      ) was differentially regulated by Ca\n                      <jats:sup>2+<\/jats:sup>\n                      across bacterial strains and host cell models. Deleting\n                      <jats:italic toggle=\"yes\">lecA<\/jats:italic>\n                      either completely or partially abolished Ca\n                      <jats:sup>2+<\/jats:sup>\n                      -dependent increase in adherence of FRD1. This impact was reversed by gene complementation. In agreement with the Ca\n                      <jats:sup>2+<\/jats:sup>\n                      -induced expression of\n                      <jats:italic toggle=\"yes\">fliC<\/jats:italic>\n                      , the proportion of flagellated PAO1 cells increased within the bacterial populations grown in the presence of Ca\n                      <jats:sup>2+<\/jats:sup>\n                      . The observed Ca\n                      <jats:sup>2+<\/jats:sup>\n                      -dependent increase in\n                      <jats:italic toggle=\"yes\">P. aeruginosa<\/jats:italic>\n                      adherence to lung epithelial cells may promote the initiation of the pathogen\u2019s infections in CF airways.\n                    <\/jats:p>\n                  <\/jats:sec>","DOI":"10.1128\/iai.00430-26","type":"journal-article","created":{"date-parts":[[2026,9,11]],"date-time":"2026-09-11T13:58:51Z","timestamp":1789135131000},"update-policy":"https:\/\/doi.org\/10.1128\/asmj-crossmark-policy-page","source":"Crossref","is-referenced-by-count":0,"title":["Calcium promotes\n                    <i>Pseudomonas aeruginosa<\/i>\n                    adherence to airway epithelial cells during 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