{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,4,9]],"date-time":"2026-04-09T03:47:15Z","timestamp":1775706435988,"version":"3.50.1"},"reference-count":47,"publisher":"Wiley","issue":"12","license":[{"start":{"date-parts":[[2016,9,6]],"date-time":"2016-09-06T00:00:00Z","timestamp":1473120000000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"funder":[{"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":[],"crossmark-restriction":false},"short-container-title":["Int Forum Allergy Rhinol"],"published-print":{"date-parts":[[2016,12]]},"abstract":"<jats:sec><jats:title>Background<\/jats:title><jats:p>Diverse microbial communities colonize healthy sinus mucosa and specific species within these communities are capable of protecting the host from pathogenic infection. However, little is known of the dynamics of upper airway infection and the role of the sinus mucosal microbiome in short\u2010 and longer\u2010term outcomes using clinical isolates from patients with chronic rhinosinusitis.<\/jats:p><\/jats:sec><jats:sec><jats:title>Methods<\/jats:title><jats:p>We examine microbiome and immune dynamics after murine sinus infection with <jats:italic>Pseudomonas aeruginosa<\/jats:italic> EC1, isolated previously from a chronic rhinosinusitis patient. Microbiota profiling (16S rRNA sequencing), histologic, and immunologic analyses [interferon\u2010gamma (IFN\u2010\u03b3) and eotaxin\u20101 (CCL11) gene expression] were performed at 1, 7, and 10 days postinfection (D1PI, D7PI, and D10PI) in antimicrobial\u2010treated and untreated animals.<\/jats:p><\/jats:sec><jats:sec><jats:title>Results<\/jats:title><jats:p>At D1PI, <jats:italic>P. aeruginosa<\/jats:italic> EC1 dominated the upper airway microbiome and was associated with a significant increase in sinus mucosa goblet cell hyperplasia, mucin hypersecretion (<jats:italic>p<\/jats:italic> &lt; 0.001), and IFN\u2010\u03b3 expression in antibiotic\u2010treated and untreated animals, although the magnitude of pathogen enrichment was lower in the latter group. Mucin hypersecretion and IFN\u2010\u03b3 expression subsided by 7D7PI in both groups of mice, coincident with a depletion of the infectious strain. However, other members of the <jats:italic>Pseudomonadaceae<\/jats:italic> family remained significantly enriched (<jats:italic>p<\/jats:italic> &lt; 0.05, <jats:italic>q<\/jats:italic> &lt; 0.05) in the microbiome at D7PI and D10PI and this perturbation was associated with induction of eotaxin\u20101 at these later time\u2010points.<\/jats:p><\/jats:sec><jats:sec><jats:title>Conclusion<\/jats:title><jats:p>Murine intranasal <jats:italic>P. aeruginosa<\/jats:italic> EC1 infection causes a pervasive shift in the sinus microbiome that persists despite histologic resolution and is associated with a reproducible immunologic shift from an initial IFN\u2010\u03b3 response to a temporal induction of eotaxin\u20101.<\/jats:p><\/jats:sec>","DOI":"10.1002\/alr.21819","type":"journal-article","created":{"date-parts":[[2016,9,6]],"date-time":"2016-09-06T14:38:09Z","timestamp":1473172689000},"page":"1229-1237","source":"Crossref","is-referenced-by-count":13,"title":["A chronic 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