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Identifying the role of NLRP3 inflammasome in stroke progression and outcome before recanalization.

Overview

Authors: Maximilian Bellut1, Alexander M Kollikowski2, Marius L Vogt2, Lukas Rossnagel3, Ibrahim Hawwari3, Bernardo S Franklin3, Mirko Pham2, Guido Stoll4, Michael K Schuhmann1
ORCID iDs: Maximilian Bellut
  1. University Hospital Würzburg, Department of Neurology, Würzburg, Germany
  2. University Hospital Würzburg, Department of Neuroradiology, Würzburg, Germany
  3. Institute of Innate Immunity, Medical Faculty, University of Bonn, Bonn, Germany
  4. University Hospital Würzburg, Institute for Experimental Biomedicine, Würzburg, Germany
Institutions: Universitätsklinikum Würzburg (Germany); University of Bonn (Germany)
Journal: Cell reports. Medicine, volume 7, issue 4, article 102723
Dates: received 1 November 2024; accepted 9 March 2026; published online 31 March 2026; in print April 2026
Type: Brief report · Language: English
License: CC BY
Identifiers: DOI 10.1016/j.xcrm.2026.102723 · PMID 41923625 · PMCID PMC13130646 · OpenAlex W7147009943
Open access: gold, a free copy (OpenAlex)
Status: code on request (how the code is found and verified)
Categories: human (organism), mouse (organism), stroke (population)
Methods: Statistics, Smoothing, state filtering, decompositions, Connectivity
Keywords: acute ischemic stroke, AIS, large vessel occlusion, LVO, NLRP3 inflammasome, endovascular thrombectomy, EVT, infarct progression, MCC950, NLRP3 inhibitor, neutrophils, interleukin 1β, pial blood sampling, middle cerebral artery occlusion, MCAO
MeSH: Inflammasomes*, NLR Family, Pyrin Domain-Containing 3 Protein*, Stroke*, Animals, Disease Progression, Furans, Humans, Indenes, Infarction, Middle Cerebral Artery, Male, Mice, Mice, Inbred C57BL, Neutrophils, Sulfonamides (* major topic)
Topic: Inflammasome and immune disorders (Molecular Biology, Biochemistry, Genetics and Molecular Biology), according to OpenAlex
Funding: Julius-Maximilians-Universität Würzburg (T-516); Else Kroner-Fresenius Foundation (2023_EKEA.187); Interdisziplinäres Zentrum für Klinische Forschung, Universitätsklinikum Würzburg
Citations: cited by 2 papers (Europe PMC); 25 references in the paper
Research resources: Anti-Albumin RRID:AB_10888110, Alexa Fluor 647 goat anti-rat IgG RRID:AB_141778, Anti-NeuN RRID:AB_2298772, RRID:AB_2340771, anti-NLRP3/NALP3 mAb (Cryo-2) RRID:AB_2490202, RRID:AB_2490248, Alexa Fluor 488 goat anti-mouse IgG RRID:AB_2534069, Alexa Fluor 546 goat anti-rabbit IgG RRID:AB_2534093, Alexa Fluor 488 donkey anti-rabbit IgG RRID:AB_2535792, Alexa Fluor 488 donkey antirat IgG RRID:AB_2535794, Alexa Fluor(R) 594 anti-mouse Ly-6G RRID:AB_2563207, Purified Mouse IgG k Isotype Ctrl RRID:AB_2801452, Gasdermin D (E9S1X) RRID:AB_2916333, Goat Anti-Mouse Il-1 beta RRID:AB_356450, Anti-CD105 RRID:AB_3718119, Anti-β-Actin Antibody RRID:AB_476744, Anti-MAP2 Polyclonal Antibody RRID:AB_776174, GraphPad StatMate 2.00 RRID:SCR_000306, GraphPad Prism 8.0.2 RRID:SCR_002798

Abstract

Acute ischemic stroke (AIS) induces a rapid inflammatory response that partly counteracts the beneficial effects of recanalization by endovascular thrombectomy (EVT). The molecular triggers of inflammation in AIS are still elusive. We analyze the role of the NOD-, LRR-, and pyrin domain-containing protein 3 (NLRP3) inflammasome before recanalization. NLRP3-mRNA levels increase rapidly in the ischemic brain following permanent middle cerebral artery occlusion in mice. NLRP3 protein is primarily expressed by intravascular neutrophils and cerebral endothelium. Blocking NLRP3 activation with the small molecule MCC950 reduces infarct progression and inflammation significantly already during large vessel occlusion. In human AIS, we find similarly increased NLRP3 expression in accumulating leukocytes within pial blood samples taken from the secluded ischemic brain territory immediately before recanalization. The number of NLRP3-positive cells before EVT predicts stroke outcome after 3 months. Our results identify NLRP3 as a promising therapeutic target to attenuate rapid infarct progression prior to recanalization.

Reproduced under the paper's license (CC BY), from the paper cited above.

Code

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Reproduced under the paper's license (CC BY), from the paper cited above.

Versions

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Version 1, 30 September 2026: the first record

Recorded: type, language, journal, volume, issue, pages, dates, 9 authors, 15 keywords, 14 MeSH terms, 3 funders, 25 references, 19 RRIDs.

Cite

This paper

Bellut, M., Kollikowski, A. M., Vogt, M. L., Rossnagel, L., Hawwari, I., Franklin, B. S., Pham, M., Stoll, G., & Schuhmann, M. K. (2026). Identifying the role of NLRP3 inflammasome in stroke progression and outcome before recanalization. Cell reports. Medicine, 7(4), 102723. https://doi.org/10.1016/j.xcrm.2026.102723

BibTeX

@article{bellut2026identifying,
author = {Bellut, Maximilian and Kollikowski, Alexander M and Vogt, Marius L and Rossnagel, Lukas and Hawwari, Ibrahim and Franklin, Bernardo S and Pham, Mirko and Stoll, Guido and Schuhmann, Michael K},
title = {{Identifying the role of NLRP3 inflammasome in stroke progression and outcome before recanalization}},
journal = {Cell reports. Medicine},
year = {2026},
month = mar,
volume = {7},
number = {4},
pages = {102723},
publisher = {Elsevier},
issn = {2666-3791},
doi = {10.1016/j.xcrm.2026.102723},
url = {https://doi.org/10.1016/j.xcrm.2026.102723},
pmid = {41923625},
pmcid = {PMC13130646}
}

RIS

TY - JOUR
AU - Bellut, Maximilian
AU - Kollikowski, Alexander M
AU - Vogt, Marius L
AU - Rossnagel, Lukas
AU - Hawwari, Ibrahim
AU - Franklin, Bernardo S
AU - Pham, Mirko
AU - Stoll, Guido
AU - Schuhmann, Michael K
TI - Identifying the role of NLRP3 inflammasome in stroke progression and outcome before recanalization
T2 - Cell reports. Medicine
J2 - Cell Rep Med
PY - 2026
DA - 2026/03/31
VL - 7
IS - 4
SP - 102723
SN - 2666-3791
PB - Elsevier
DO - 10.1016/j.xcrm.2026.102723
UR - https://doi.org/10.1016/j.xcrm.2026.102723
LA - en
ER -

CSL-JSON

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