Dataset Information

Human sepsis with plasma samples

ABSTRACT: The project examines the mechanisms of neutrophil dysfunction during sepsis. Our work uncovered the central role of cell free circulating histones in eliminating mature neutrophil in favour of immature cells and characterized the mechanisms that regulate their release following systemic infection. Mature and immature neutrophil Ly6Ghigh and Ly6Glow populations isolated from the spleens of WT and TCRα-deficient mice either naïve or infected with C. albicans were characterized. In addition, these populations were compared to neutrophils isolated from WT mice receiving Clodronate-liposomes and recombinant G-CSF. These studies demonstrated that T-cell derived histones drive the release of G-CSF in the spleen and progressively eliminate mature neutrophils by shortening their lifespan. Finally, we conducted proteomic analysis of plasmas isolated from patients with microbial sepsis to correlate markers of neutrophil death to plasma cytokine and histone levels, confirming the pathogenic role these molecules play during sepsis in humans.

INSTRUMENT(S): TripleTOF 5600

ORGANISM(S): Homo Sapiens (human)

TISSUE(S): Blood Plasma

SUBMITTER: Spyros Vernardis

LAB HEAD: Markus Ralser

PROVIDER: PXD034391 | Pride | 2022-07-01

REPOSITORIES: Pride

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Publications

Microbe capture by splenic macrophages triggers sepsis via T cell-death-dependent neutrophil lifespan shortening.

Ioannou Marianna M Hoving Dennis D Aramburu Iker Valle IV Temkin Mia I MI De Vasconcelos Nathalia M NM Tsourouktsoglou Theodora-Dorita TD Wang Qian Q Boeing Stefan S Goldstone Robert R Vernardis Spyros S Demichev Vadim V Ralser Markus M David Sascha S Stahl Klaus K Bode Christian C Papayannopoulos Venizelos V

Nature communications 20220809 1

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 myeloperoxidas ...[more]

PMID: 35945238

			Action	DRS
	MSQC_1.wiff	Wiff
	MSQC_1.wiff.scan	Wiff
	MSQC_10.wiff	Wiff
	MSQC_10.wiff.scan	Wiff
	MSQC_11.wiff	Wiff

Dataset Information

Human sepsis with plasma samples

Dataset's files

Publications

Microbe capture by splenic macrophages triggers sepsis via T cell-death-dependent neutrophil lifespan shortening.

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