{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,18]],"date-time":"2026-09-18T05:52:20Z","timestamp":1789710740251,"version":"4.0.1"},"reference-count":64,"publisher":"Frontiers Media SA","license":[{"start":{"date-parts":[[2026,6,11]],"date-time":"2026-06-11T00:00:00Z","timestamp":1781136000000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"funder":[{"DOI":"10.13039\/100000050","name":"National Heart, Lung, and Blood Institute","doi-asserted-by":"publisher","id":[{"id":"10.13039\/100000050","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000897","name":"Cystic Fibrosis Foundation","doi-asserted-by":"publisher","id":[{"id":"10.13039\/100000897","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["frontiersin.org"],"crossmark-restriction":true},"short-container-title":["Front. Tuberc."],"abstract":"\n Introduction<\/jats:title>\n \n Mycobacterium abscessus<\/jats:italic>\n (\n Mabsc<\/jats:italic>\n ), a nontuberculous mycobacterium (NTM), is readily cleared from healthy lungs but can cause infections in immunocompromised individuals and individuals with chronic airways diseases that disrupt mucociliary clearance, such as cystic fibrosis and bronchiectasis. In bronchiectatic airways,\n Mabsc<\/jats:italic>\n can persist despite robust immune cell recruitment, raising the possibility that, in addition to impaired mucociliary clearance, local pulmonary immune defects contribute to NTM susceptibility. Since chronic infections result from failed eradication of acute infection, we sought to determine whether immune cell responses critical for control of acute\n Mabsc<\/jats:italic>\n infection in healthy lungs remain relevant when\n Mabsc<\/jats:italic>\n infection occurs in obstructed airways, rather than in the alveoli, as occurs in bronchiectasis.\n <\/jats:p>\n <\/jats:sec>\n \n Methods<\/jats:title>\n \n Using an agar bead model of\n Mabsc<\/jats:italic>\n infection that prolongs murine small airway infection, replicates factors associated with bronchiectasis, and mirrors pathology of human\n Mabsc<\/jats:italic>\n lung disease, we tested the hypothesis that\n Mabsc<\/jats:italic>\n infection in obstructed airways elicits a qualitatively different immune response that alveolar\n Mabsc<\/jats:italic>\n infection. We compared myeloid cell responses in in the two infection models using flow cytometric analyses of lung cells, immunofluorescent imaging, and histopathologic evaluation of lung sections.\n <\/jats:p>\n <\/jats:sec>\n \n Results<\/jats:title>\n \n During the first 2 weeks of the bead model of\n Mabsc<\/jats:italic>\n infection, absolute abundance of neutrophils in the lungs was significantly higher and relative abundance of recruited macrophages was lower than in the alveolar\n Mabsc<\/jats:italic>\n infection model. Additionally, most resident alveolar macrophages (CD11c\n +<\/jats:sup>\n RAMs) in the bead model upregulated CD11b, a marker of inflammation, by 1-week post-infection and maintained high levels of CD11b expression at 3 weeks post infection despite infection occurring in airways, not alveoli. To understand the role of macrophage subsets in controlling\n Mabsc<\/jats:italic>\n infection, clodronate liposomes were administered oropharyngeally to deplete RAMs. RAMs were essential for early control of alveolar\n Mabsc<\/jats:italic>\n infection, but depletion of RAMs had no effect on control of\n Mabsc<\/jats:italic>\n burden during bead infection.\n <\/jats:p>\n <\/jats:sec>\n \n Conclusions<\/jats:title>\n \n These studies demonstrate that murine\n Mabsc<\/jats:italic>\n airway infection induced by obstructing small airways with\n Mabsc<\/jats:italic>\n embedded in agar beads generates an immune milieu distinct from that induced by\n Mabsc<\/jats:italic>\n infection in alveoli, altering the importance of different macrophage populations for control of infection.\n <\/jats:p>\n 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