{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Ioannou M"],"funding":["European Molecular Biology Organization","Cancer Research UK","Francis Crick Institute","The Francis Crick Institute","Medical Research Council","Wellcome Trust"],"pagination":["4658"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC9361272"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["13(1)"],"pubmed_abstract":["The mechanisms linking systemic infection to hyperinflammation and immune dysfunction in sepsis are poorly understood. Extracellular histones promote sepsis pathology, but their source and mechanism of action remain unclear. Here, we show that by controlling fungi and bacteria captured by splenic macrophages, neutrophil-derived myeloperoxidase attenuates sepsis by suppressing histone release. In systemic candidiasis, microbial capture via the phagocytic receptor SIGNR1 neutralizes myeloperoxidase by facilitating marginal zone infiltration and T cell death-dependent histone release. Histones and hyphae induce cytokines in adjacent CD169 macrophages including G-CSF that selectively depletes mature Ly6G<sup>high</sup> neutrophils by shortening their lifespan in favour of immature Ly6G<sup>low"],"journal":["Nature communications"],"pubmed_title":["Microbe capture by splenic macrophages triggers sepsis via T cell-death-dependent neutrophil lifespan shortening."],"pmcid":["PMC9361272"],"funding_grant_id":["10129","ALTF 113-2019","CC2089","CC1064","FC001134","10134","10001","CC1107","SHWF 222825/Z/21/Z","FC0010129","222825/Z/21/Z"],"pubmed_authors":["Demichev V","Aramburu IV","Hoving D","Boeing S","Temkin MI","De Vasconcelos NM","Stahl K","Papayannopoulos V","Wang Q","Ioannou M","Tsourouktsoglou TD","Vernardis S","David S","Bode C","Ralser M","Goldstone R"],"additional_accession":[]},"is_claimable":false,"name":"Microbe capture by splenic macrophages triggers sepsis via T cell-death-dependent neutrophil lifespan shortening.","description":"The mechanisms linking systemic infection to hyperinflammation and immune dysfunction in sepsis are poorly understood. Extracellular histones promote sepsis pathology, but their source and mechanism of action remain unclear. Here, we show that by controlling fungi and bacteria captured by splenic macrophages, neutrophil-derived myeloperoxidase attenuates sepsis by suppressing histone release. In systemic candidiasis, microbial capture via the phagocytic receptor SIGNR1 neutralizes myeloperoxidase by facilitating marginal zone infiltration and T cell death-dependent histone release. Histones and hyphae induce cytokines in adjacent CD169 macrophages including G-CSF that selectively depletes mature Ly6G<sup>high</sup> neutrophils by shortening their lifespan in favour of immature Ly6G<sup>low","dates":{"release":"2022-01-01T00:00:00Z","publication":"2022 Aug","modification":"2026-05-09T19:29:03.58Z","creation":"2025-02-19T03:23:25.19Z"},"accession":"S-EPMC9361272","cross_references":{"pubmed":["35945238"],"doi":["10.1038/s41467-022-32320-1"]}}