{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,6]],"date-time":"2026-10-06T15:53:54Z","timestamp":1791302034968,"version":"4.1.0"},"reference-count":58,"publisher":"Oxford University Press (OUP)","issue":"6","license":[{"start":{"date-parts":[[2005,3,1]],"date-time":"2005-03-01T00:00:00Z","timestamp":1109635200000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/academic.oup.com\/pages\/standard-publication-reuse-rights"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[2005,3,15]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:p>Clearance of neutrophils from inflamed sites is critical for resolution of inflammation, but pathogen-driven neutrophil apoptosis can impair host defenses. We previously showed that pyocyanin, a phenazine toxic metabolite produced by Pseudomonas aeruginosa, accelerates neutrophil apoptosis in vitro. We compared wild-type and pyocyanin-deficient strains of P. aeruginosa in a murine model of acute pneumonia. Intratracheal instillation of either strain of P. aeruginosa caused a rapid increase in bronchoalveolar lavage neutrophil counts up to 18 h after infection. In wild-type infection, neutrophil numbers then declined steadily, whereas neutrophil numbers increased up to 48 h in mice infected with pyocyanin-deficient P. aeruginosa. In keeping with these differences, pyocyanin production was associated with reduced bacterial clearance from the lungs. Neutrophil apoptosis was increased in mice infected with wild-type compared with the phenazine-deficient strain or two further strains that lack pyocyanin production, but produce other phenazines. Concentrations of potent neutrophil chemokines (MIP-2, KC) and cytokines (IL-6, IL-1\u03b2) were significantly lower in wild-type compared with phenazine-deficient strain-infected mice at 18 h. We conclude that pyocyanin production by P. aeruginosa suppresses the acute inflammatory response by pathogen-driven acceleration of neutrophil apoptosis and by reducing local inflammation, and that this is advantageous for bacterial survival.<\/jats:p>","DOI":"10.4049\/jimmunol.174.6.3643","type":"journal-article","created":{"date-parts":[[2014,4,21]],"date-time":"2014-04-21T22:13:50Z","timestamp":1398118430000},"page":"3643-3649","source":"Crossref","is-referenced-by-count":229,"title":["Pyocyanin Production by\n                    <i>Pseudomonas aeruginosa<\/i>\n                    Induces Neutrophil Apoptosis and Impairs Neutrophil-Mediated Host Defenses In Vivo"],"prefix":"10.1093","volume":"174","author":[{"given":"Lucy","family":"Allen","sequence":"first","affiliation":[{"name":"Cardiovascular Research Unit, Division of Clinical Sciences (North), University of Sheffield , Sheffield ,","place":["United Kingdom"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"David H","family":"Dockrell","sequence":"additional","affiliation":[{"name":"Academic Units of Infectious Diseases, University of Sheffield , Sheffield ,","place":["United Kingdom"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Theresa","family":"Pattery","sequence":"additional","affiliation":[{"name":"Laboratory of Microbial Interactions, Department of Molecular and Cellular Interactions, Flanders Interuniversity Institute of Biotechnology, Vrije Universiteit Brussels , Brussels ,","place":["Belgium"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Daniel G","family":"Lee","sequence":"additional","affiliation":[{"name":"Department of Molecular Biology, Massachusetts General Hospital , Wellman 10, Boston, MA 02114"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Pierre","family":"Cornelis","sequence":"additional","affiliation":[{"name":"Laboratory of Microbial Interactions, Department of Molecular and Cellular Interactions, Flanders Interuniversity Institute of Biotechnology, Vrije Universiteit Brussels , Brussels ,","place":["Belgium"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Paul G","family":"Hellewell","sequence":"additional","affiliation":[{"name":"Cardiovascular Research Unit, Division of Clinical Sciences (North), University of Sheffield , Sheffield ,","place":["United Kingdom"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Moira K B","family":"Whyte","sequence":"additional","affiliation":[{"name":"Academic Units of Respiratory Medicine, Division of Genomic Medicine, University of Sheffield , Sheffield ,","place":["United Kingdom"]}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"286","published-online":{"date-parts":[[2005,3,15]]},"reference":[{"key":"2026020213025715900_R1","first-page":"669","volume-title":"Br. 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