{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,8,7]],"date-time":"2026-08-07T20:05:05Z","timestamp":1786133105458,"version":"build-2736575974"},"reference-count":41,"publisher":"Ovid Technologies (Wolters Kluwer Health)","issue":"7","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["JASN"],"published-print":{"date-parts":[[2017,7]]},"abstract":"<jats:p>\n                    Bacterial peritonitis remains the main cause of technique failure in peritoneal dialysis (PD). During peritonitis, the peritoneal membrane undergoes structural and functional alterations that are mediated by IL-1\n                    <jats:italic toggle=\"yes\">\u03b2<\/jats:italic>\n                    . The NLRP3 inflammasome is a caspase-1\u2013activating multiprotein complex that links sensing of microbial and stress products to activation of proinflammatory cytokines, including IL-1\n                    <jats:italic toggle=\"yes\">\u03b2<\/jats:italic>\n                    . The potential roles of the NLRP3 inflammasome and IL-1\n                    <jats:italic toggle=\"yes\">\u03b2<\/jats:italic>\n                    in the peritoneal membrane during acute peritonitis have not been investigated. Here, we show that the NLRP3 inflammasome is activated during acute bacterial peritonitis in patients on PD, and this activation associates with the release of IL-1\n                    <jats:italic toggle=\"yes\">\u03b2<\/jats:italic>\n                    in the dialysate. In mice, lipopolysaccharide- or\n                    <jats:italic toggle=\"yes\">Escherichia coli<\/jats:italic>\n                    -induced peritonitis led to IL-1\n                    <jats:italic toggle=\"yes\">\u03b2<\/jats:italic>\n                    release in the peritoneal membrane. The genetic deletion of\n                    <jats:italic toggle=\"yes\">Nalp3<\/jats:italic>\n                    , which encodes NLRP3, abrogated defects in solute transport during acute peritonitis and restored ultrafiltration. In human umbilical vein endothelial cells, IL-1\n                    <jats:italic toggle=\"yes\">\u03b2<\/jats:italic>\n                    treatment directly enhanced endothelial cell proliferation and increased microvascular permeability. These\n                    <jats:italic toggle=\"yes\">in vitro<\/jats:italic>\n                    effects require endothelial IL-1 receptors, shown by immunofluorescence to be expressed in peritoneal capillaries in mice. Furthermore, administration of the IL-1\n                    <jats:italic toggle=\"yes\">\u03b2<\/jats:italic>\n                    receptor antagonist, anakinra, efficiently decreased nitric oxide production and vascular proliferation and restored peritoneal function in mouse models of peritonitis, even in mice treated with standard-of-care antibiotherapy. These data demonstrate that NLRP3 activation and IL-1\n                    <jats:italic toggle=\"yes\">\u03b2<\/jats:italic>\n                    release have a critical role in solute transport defects and tissue remodeling during PD-related peritonitis. Blockade of the NLRP3\/IL-1\n                    <jats:italic toggle=\"yes\">\u03b2<\/jats:italic>\n                    axis offers a novel method for rescuing morphologic alterations and transport defects during acute peritonitis.\n                  <\/jats:p>","DOI":"10.1681\/asn.2016070729","type":"journal-article","created":{"date-parts":[[2017,2,13]],"date-time":"2017-02-13T20:20:14Z","timestamp":1487017214000},"page":"2038-2052","source":"Crossref","is-referenced-by-count":43,"title":["The NLRP3 Inflammasome Has a Critical Role in Peritoneal Dialysis-Related Peritonitis"],"prefix":"10.1681","volume":"28","author":[{"given":"Nicolas","family":"Hautem","sequence":"first","affiliation":[{"name":"Institut de Recherche Exp\u00e9rimentale et Clinique, Universit\u00e9 catholique de Louvain, Brussels, Belgium;"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Johann","family":"Morelle","sequence":"additional","affiliation":[{"name":"Institut de Recherche Exp\u00e9rimentale et Clinique, Universit\u00e9 catholique de Louvain, Brussels, Belgium;"},{"name":"Division of Nephrology, Cliniques universitaires Saint-Luc, Brussels, Belgium; and"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Amadou","family":"Sow","sequence":"additional","affiliation":[{"name":"Institut de Recherche Exp\u00e9rimentale et Clinique, Universit\u00e9 catholique de Louvain, Brussels, Belgium;"},{"name":"Division of Nephrology, Cliniques universitaires Saint-Luc, Brussels, Belgium; and"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Cyril","family":"Corbet","sequence":"additional","affiliation":[{"name":"Institut de Recherche Exp\u00e9rimentale et Clinique, Universit\u00e9 catholique de Louvain, Brussels, Belgium;"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Olivier","family":"Feron","sequence":"additional","affiliation":[{"name":"Institut de Recherche Exp\u00e9rimentale et Clinique, Universit\u00e9 catholique de Louvain, Brussels, Belgium;"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Eric","family":"Goffin","sequence":"additional","affiliation":[{"name":"Division of Nephrology, Cliniques universitaires Saint-Luc, Brussels, Belgium; and"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Fran\u00e7ois","family":"Huaux","sequence":"additional","affiliation":[{"name":"Institut de Recherche Exp\u00e9rimentale et Clinique, Universit\u00e9 catholique de Louvain, Brussels, Belgium;"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Olivier","family":"Devuyst","sequence":"additional","affiliation":[{"name":"Institut de Recherche Exp\u00e9rimentale et Clinique, Universit\u00e9 catholique de Louvain, Brussels, Belgium;"},{"name":"Division of Nephrology, Cliniques universitaires Saint-Luc, Brussels, Belgium; and"},{"name":"Institute of Physiology, University of Zurich, Zurich, Switzerland"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"276","published-online":{"date-parts":[[2017,2,13]]},"reference":[{"key":"B1-20230829","doi-asserted-by":"crossref","first-page":"3238","DOI":"10.1681\/ASN.2016010112","article-title":"The Current state of peritoneal dialysis.","volume":"27","author":"Mehrotra","year":"2016","journal-title":"J Am Soc Nephrol"},{"key":"B2-20230829","doi-asserted-by":"crossref","first-page":"278","DOI":"10.1053\/j.ajkd.2014.02.025","article-title":"Peritoneal dialysis-related peritonitis: Towards improving evidence, practices, and outcomes.","volume":"64","author":"Cho","year":"2014","journal-title":"Am J Kidney Dis"},{"key":"B3-20230829","doi-asserted-by":"crossref","first-page":"639","DOI":"10.3747\/pdi.2010.00185","article-title":"Peritoneal dialysis-associated peritonitis rates and outcomes in a national cohort are not improving in the post-millennium 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