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The DOI matches its Crossref record; 11 of the 11 references it cites were found in a registry or an index.

Intravenous immunoglobulin suppresses NLRP1 and NLRP3 inflammasome-mediated neuronal death in ischemic stroke

Open access
Yang-Wei Fann, D, Lee, S-Y, Manzanero, S, Tang, S-C, Gelderblom, M, Chunduri, P, Bernreuther, C, Glatzel, M, Cheng, Y-L, Thundyil, J, Widiapradja, A, Lok, K-Z, Foo, S L, Wang, Y-C, Li, Y-I, Drummond, G R, Basta, M, Magnus, T, Jo, D-G, Mattson, M P, Sobey, C G, Arumugam, T V·2013·Cell Death & Disease
DOI 10.1038/cddis.2013.326
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Abstract

Multi-protein complexes called inflammasomes have recently been identified and shown to contribute to cell death in tissue injury. Intravenous immunoglobulin (IVIg) is an FDA-approved therapeutic modality used for various inflammatory diseases. The objective of this study is to investigate dynamic responses of the NLRP1 and NLRP3 inflammasomes in stroke and to determine whether the NLRP1 and NLRP3 inflammasomes can be targeted with IVIg for therapeutic intervention. Primary cortical neurons were subjected to glucose deprivation (GD), oxygen-glucose deprivation (OGD) or simulated ischemia-reperfusion (I/R). Ischemic stroke was induced in C57BL/6J mice by middle cerebral artery occlusion, followed by reperfusion. Neurological assessment was performed, brain tissue damage was quantified, and NLRP1 and NLRP3 inflammasome protein levels were evaluated. NLRP1 and NLRP3 inflammasome components were also analyzed in postmortem brain tissue samples from stroke patients. Ischemia-like conditions increased the levels of NLRP1 and NLRP3 inflammasome proteins, and IL-1β and IL-18, in primary cortical neurons. Similarly, levels of NLRP1 and NLRP3 inflammasome proteins, IL-1β and IL-18 were elevated in ipsilateral brain tissues of cerebral I/R mice and stroke patients. Caspase-1 inhibitor treatment protected cultured cortical neurons and brain cells in vivo in experimental stroke models. IVIg treatment protected neurons in experimental stroke models by a mechanism involving suppression of NLRP1 and NLRP3 inflammasome activity. Our findings provide evidence that the NLRP1 and NLRP3 inflammasomes have a major role in neuronal cell death and behavioral deficits in stroke. We also identified NLRP1 and NLRP3 inflammasome inhibition as a novel mechanism by which IVIg can protect brain cells against ischemic damage, suggesting a potential clinical benefit of therapeutic interventions that target inflammasome assembly and activity.

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Metadata

Authors
Yang-Wei Fann, D., Lee, S.-Y., Manzanero, S., Tang, S.-C., Gelderblom, M., Chunduri, P., Bernreuther, C., Glatzel, M., Cheng, Y.-L., Thundyil, J., Widiapradja, A., Lok, K.-Z., Foo, S. L., Wang, Y.-C., Li, Y.-I., Drummond, G. R., Basta, M., Magnus, T., Jo, D.-G., Mattson, M. P., Sobey, C. G., & Arumugam, T. V.
Venue
Cell Death & Disease
Publisher
Springer Science and Business Media LLC
Published
2013-09-05
Volume
4
Issue
9
Pages
e790-e790
ISSN
2041-4889 (ISSN-L)
DOI
10.1038/cddis.2013.326
OpenAlex
W2030345966
Cited by
475
References
11
FWCI
11.97
Type
journal article
Language
en
Open access
gold

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CoChat. (2026). Citation check: Intravenous immunoglobulin suppresses NLRP1 and NLRP3 inflammasome-mediated neuronal death in ischemic stroke. https://app.cochat.ai/papers/10.1038/cddis.2013.326
The paper
Yang-Wei Fann, D., Lee, S.-Y., Manzanero, S., Tang, S.-C., Gelderblom, M., Chunduri, P., Bernreuther, C., Glatzel, M., Cheng, Y.-L., Thundyil, J., Widiapradja, A., Lok, K.-Z., Foo, S. L., Wang, Y.-C., Li, Y.-I., Drummond, G. R., Basta, M., Magnus, T., Jo, D.-G., . . . Arumugam, T. V. (2013). Intravenous immunoglobulin suppresses NLRP1 and NLRP3 inflammasome-mediated neuronal death in ischemic stroke. Cell Death & Disease. https://doi.org/10.1038/cddis.2013.326

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Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).

Semantic Scholar’s data is described in: Kinney, R., et al. (2023). The Semantic Scholar Open Data Platform. arXiv:2301.10140.