{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,21]],"date-time":"2026-10-21T15:49:06Z","timestamp":1792597746785,"version":"4.5.0"},"reference-count":196,"publisher":"Frontiers Media SA","license":[{"start":{"date-parts":[[2026,6,3]],"date-time":"2026-06-03T00:00:00Z","timestamp":1780444800000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"funder":[{"DOI":"10.13039\/100000060","name":"National Institute of Allergy and Infectious Diseases","doi-asserted-by":"publisher","id":[{"id":"10.13039\/100000060","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["frontiersin.org"],"crossmark-restriction":true},"short-container-title":["Front. Cell. Infect. Microbiol."],"abstract":"<jats:p>\n                    Chronic bacterial respiratory infections by\n                    <jats:italic>Staphylococcus aureus<\/jats:italic>\n                    are a hallmark of cystic fibrosis (CF) lung disease, affecting up to 80% of all people with CF by their mid-teens.\n                    <jats:italic>S. aureus<\/jats:italic>\n                    is able to survive and persist in the CF lung despite robust neutrophilic inflammation. As neutrophils are the immune system\u2019s front line of defense against bacteria, the persistent nature of\n                    <jats:italic>S. aureus<\/jats:italic>\n                    infections in CF indicates both a defect in the ability of neutrophils to kill\n                    <jats:italic>S. aureus<\/jats:italic>\n                    and an enhanced ability of the bacteria to survive.\n                    <jats:italic>S. aureus<\/jats:italic>\n                    persistence in the CF lung is driven by both microbial and host, genetic and microenvironmental, factors. There doesn\u2019t seem to be one unifying feature that makes\n                    <jats:italic>S. aureus<\/jats:italic>\n                    more virulent in the CF lung as several factors have been proposed to aide its survival. These include increased resistance to antibiotics, the ability to form small colony variants, biofilm formation, co-infection with\n                    <jats:italic>Pseudomonas aeruginosa<\/jats:italic>\n                    , and several virulence factors such as the accessory gene regulatory system, leukocidins, and staphylococcal protein A. A variety of host factors also affect the ability of neutrophils to kill\n                    <jats:italic>S. aureus<\/jats:italic>\n                    in the CF lung. Defects in the function of the cystic fibrosis transmembrane conductance regulator, the genetic cause of CF, affect phagolysosomal killing and lead to increased formation of neutrophil extracellular traps, which are less effective at killing\n                    <jats:italic>S. aureus<\/jats:italic>\n                    . Additionally, data suggest that factors within the CF lung microenvironment also affect neutrophilic killing of\n                    <jats:italic>S. aureus<\/jats:italic>\n                    . However, more research is needed to clearly identify what these environmental factors may be. This review article summarizes the current knowledge on the clinical relevance of\n                    <jats:italic>S. aureus<\/jats:italic>\n                    lung infections in CF, on microbial and host mechanisms promoting\n                    <jats:italic>S. aureus<\/jats:italic>\n                    survival in the CF lung, and on details of neutrophil-\n                    <jats:italic>S. aureus<\/jats:italic>\n                    interactions in CF. By understanding how\n                    <jats:italic>S. aureus<\/jats:italic>\n                    is able to survive in the CF lung and why neutrophils are unable to kill this bacterium, it could be possible to identify potential therapeutic targets to alleviate the consequences of\n                    <jats:italic>S. aureus<\/jats:italic>\n                    respiratory infection in CF.\n                  <\/jats:p>","DOI":"10.3389\/fcimb.2026.1797869","type":"journal-article","created":{"date-parts":[[2026,6,3]],"date-time":"2026-06-03T06:01:50Z","timestamp":1780466510000},"update-policy":"https:\/\/doi.org\/10.3389\/crossmark-policy","source":"Crossref","is-referenced-by-count":1,"title":["Microbial and host innate immune factors affecting the persistence of Staphylococcus aureus in cystic fibrosis airways"],"prefix":"10.3389","volume":"16","author":[{"given":"Jacob D.","family":"Fairholm","sequence":"first","affiliation":[{"name":"Department of Infectious Diseases, College of Veterinary Medicine, The University of Georgia","place":["Athens, GA, United States"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Gavin Thomas","family":"Paul","sequence":"additional","affiliation":[{"name":"Department of Infectious Diseases, College of Veterinary Medicine, The University of Georgia","place":["Athens, GA, United States"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Susan","family":"Birket","sequence":"additional","affiliation":[{"name":"Division of Pulmonary, Allergy, and Critical Care Medicine, The University of Alabama at Birmingham","place":["Birmingham, AL, United States"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Bal\u00e1zs","family":"Rada","sequence":"additional","affiliation":[{"name":"Department of Infectious Diseases, College of Veterinary Medicine, The University of Georgia","place":["Athens, GA, United States"]}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"1965","published-online":{"date-parts":[[2026,6,3]]},"reference":[{"key":"B1","doi-asserted-by":"publisher","first-page":"67","DOI":"10.1186\/s12890-015-0062-7","article-title":"Clinical outcomes associated with Staphylococcus aureus and Pseudomonas aeruginosa airway infections in adult cystic fibrosis patients","volume":"15","author":"Ahlgren","year":"2015","journal-title":"BMC Pulmonary Med."},{"key":"B2","doi-asserted-by":"publisher","first-page":"2308","DOI":"10.1016\/j.freeradbiomed.2012.10.542","article-title":"Chloride transport in functionally active phagosomes isolated from human neutrophils","volume":"53","author":"Aiken","year":"2012","journal-title":"Free Radic. 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