{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,3,11]],"date-time":"2026-03-11T03:57:45Z","timestamp":1773201465796,"version":"3.50.1"},"reference-count":53,"publisher":"Oxford University Press (OUP)","issue":"3","license":[{"start":{"date-parts":[[2024,3,14]],"date-time":"2024-03-14T00:00:00Z","timestamp":1710374400000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/academic.oup.com\/pages\/standard-publication-reuse-rights"}],"funder":[{"DOI":"10.13039\/100000002","name":"National Institutes of Health","doi-asserted-by":"publisher","award":["R01GM129633"],"award-info":[{"award-number":["R01GM129633"]}],"id":[{"id":"10.13039\/100000002","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000002","name":"National Institutes of Health","doi-asserted-by":"publisher","award":["U01AI170018"],"award-info":[{"award-number":["U01AI170018"]}],"id":[{"id":"10.13039\/100000002","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[2024,9,2]]},"abstract":"<jats:title>Abstract<\/jats:title>\n               <jats:p>B-1a cells, a regulatory subset of B lymphocytes, produce natural IgM and interleukin-10. Neutrophil extracellular traps (NETs) play a crucial role in pathogen defense, but their excessive formation during sepsis can cause further inflammation and tissue damage. In sepsis, extracellular cold-inducible RNA-binding protein (eCIRP), a damage-associated molecular pattern, is released to induce NET formation. We hypothesize that B-1a cells clear NETs to prevent sepsis-induced injury. Sepsis in mice was induced by injecting 1 \u00d7 107 and 5 \u00d7 107 colony-forming units of Escherichia coli intraperitoneally. After 4 and 20\u2005h, we assessed the number of B-1a cells in the peritoneal cavity using flow cytometry. Our results showed that the number of peritoneal B-1a cells was significantly decreased in E. coli sepsis mice. Importantly, replenishing B-1a cells via intraperitoneal injection in sepsis mice significantly decreased NETs in peritoneal neutrophils. We also observed a decrease in serum inflammation and injury markers and a significant increase in the overall survival rate in B-1a cell\u2013treated septic mice. To understand the mechanism, we cocultured bone marrow\u2013derived neutrophils with peritoneal B-1a cells in a contact or noncontact condition using an insert and stimulated them with eCIRP. After 4\u2005h, we found that eCIRP significantly increased NET formation in bone marrow\u2013derived neutrophils. Interestingly, we observed that B-1a cells inhibited NETs by 67% in a contact-dependent manner. Surprisingly, when B-1a cells were cultured in inserts, there was no significant decrease in NET formation, suggesting that direct cell-to-cell contact is crucial for this inhibitory effect. We further determined that B-1a cells promoted NET phagocytosis, and this was mediated through natural IgM, as blocking the IgM receptor attenuated the engulfment of NETs by B-1a cells. Finally, we identified that following their engulfment, NETs were localized into the lysosomal compartment for lysis. Thus, our study suggests that B-1a cells decrease NET content in eCIRP-treated neutrophils and E. coli sepsis mice.<\/jats:p>","DOI":"10.1093\/jleuko\/qiae066","type":"journal-article","created":{"date-parts":[[2024,3,14]],"date-time":"2024-03-14T19:32:24Z","timestamp":1710444744000},"page":"632-643","source":"Crossref","is-referenced-by-count":6,"title":["B-1a cells scavenge NETs to attenuate sepsis"],"prefix":"10.1093","volume":"116","author":[{"given":"Kensuke","family":"Murata","sequence":"first","affiliation":[{"name":"Center for Immunology and Inflammation, Feinstein Institutes for Medical Research , 350 Community Drive, Manhasset, NY 11030 , United States"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Atsushi","family":"Murao","sequence":"additional","affiliation":[{"name":"Center for Immunology and Inflammation, Feinstein Institutes for Medical Research , 350 Community Drive, Manhasset, NY 11030 , United 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