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Neutrophil extracellular traps melt Peyer’s patches following stroke and myocardial infarction

ABSTRACT: Sterile tissue injury after stroke causes lymphocyte contraction in lymphoid tissues and may decrease circulating IgA-levels. Intestinal Peyer’s patches (PP) harbor large numbers of IgA+ B cell precursors and plasma cells. Whether and how tissue injury triggers PP-B cell death, thereby mediating IgA-loss, is unknown. We found decreased circulating IgA levels in stroke and myocardial infarction patients. Experimental stroke and myocardial infarction in mice phenocopied the human situation. Decreased plasma and fecal IgA were accompanied by rapid and macroscopic shrinkage of PP caused by substantial losses of PP-resident IgA+ precursors and plasma cells in mice. Tissue injury induced neutrophil activation endowed with the release of toxic neutrophil extracellular traps (NETs). Antibody-mediated or genetically- induced neutrophil loss, digestion of NETs, or inhibition of their release by the Gasdermin D blockade completely prevented lymphocyte loss and PP shrinkage. We also identified NETs in the plasma of stroke and myocardial infarction patients. Hence, tissue injury induces systemic NET-release, which might be targeted to maintain immune homeostasis at mucosal barriers.

INSTRUMENT(S): Orbitrap Eclipse

ORGANISM(S): Mus Musculus (mouse)

TISSUE(S): B Cell, Neutrophil, Blood

DISEASE(S): Stroke

SUBMITTER: Susmita Ghosh

LAB HEAD: Prof. Dr. Albert Sickmann

PROVIDER: PXD044644 | Pride | 2024-02-28

REPOSITORIES: Pride

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			Action	DRS
	Bcell_strokevssham.pep.xml	Pepxml
	Eclipse_02393.raw	Raw
	Eclipse_02394.raw	Raw
	Eclipse_02395.raw	Raw
	Eclipse_02396.raw	Raw

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