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Neutrophil apoptosis is a key factor in inflammation resolution and is controlled by cytosolic proliferating cell nuclear antigen (PCNA). p21\/Waf1, a cyclin-dependent kinase inhibitor, is a partner of PCNA, and its mRNA is up-regulated in human neutrophils during LPS challenge. We show here that, after 7 days of persistent infection with P. aeruginosa, neutrophilic inflammation was more prominent in p21\u2212\/\u2212 compared with wild-type (WT) mice. Notably, no intrinsic defect in the phagocytosis of apoptotic cells by macrophages was found in p21\u2212\/\u2212 compared with WT mice. Inflammatory cell analysis in peritoneal lavages after zymosan-induced peritonitis showed a significantly increased number of neutrophils at 48 hours in p21\u2212\/\u2212 compared with WT mice. In vitro analysis was consistent with delayed neutrophil apoptosis in p21\u2212\/\u2212 compared with WT mice. Ectopic expression of p21\/waf1 in neutrophil-differentiated PLB985 cells potentiated apoptosis and reversed the prosurvival effect of PCNA. In human neutrophils, p21 messenger RNA was induced by TNF-\u03b1, granulocyte colony\u2013stimulating factor, and LPS. Neutrophils isolated from patients with CF showed enhanced survival, which was reduced after treatment with a carboxy-peptide derived from the sequence of p21\/waf1. Notably, p21\/waf1 was detected by immunohistochemistry in neutrophils within lungs from patients with CF. Our data reveal a novel role for p21\/waf1 in the resolution of inflammation via its ability to control neutrophil apoptosis. This mechanism may be relevant in the neutrophil-dominated inflammation observed in CF and other chronic inflammatory lung conditions.<\/jats:p>","DOI":"10.1165\/rcmb.2015-0047oc","type":"journal-article","created":{"date-parts":[[2015,10,30]],"date-time":"2015-10-30T14:19:17Z","timestamp":1446214757000},"page":"740-750","source":"Crossref","is-referenced-by-count":24,"title":["Neutrophil-Expressed p21\/waf1 Favors Inflammation Resolution in\n                    <i>Pseudomonas aeruginosa<\/i>\n                    Infection"],"prefix":"10.1093","volume":"54","author":[{"given":"Cl\u00e9mence","family":"Martin","sequence":"first","affiliation":[{"name":"Universit\u00e9 Paris Descartes, Sorbonne Paris Cit\u00e9, Paris, France"},{"name":"Department of Pneumology, Cochin Hospital, France"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Delphine","family":"Ohayon","sequence":"additional","affiliation":[{"name":"Universit\u00e9 Paris Descartes, Sorbonne Paris Cit\u00e9, Paris, 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