The DOI matches its Crossref record; 13 of the 13 references it cites were found in a registry or an index.
Caspase-11–mediated endothelial pyroptosis underlies endotoxemia-induced lung injury
Open accessAbstract
Acute lung injury is a leading cause of death in bacterial sepsis due to the wholesale destruction of the lung endothelial barrier, which results in protein-rich lung edema, influx of proinflammatory leukocytes, and intractable hypoxemia. Pyroptosis is a form of programmed lytic cell death that is triggered by inflammatory caspases, but little is known about its role in EC death and acute lung injury. Here, we show that systemic exposure to the bacterial endotoxin lipopolysaccharide (LPS) causes severe endothelial pyroptosis that is mediated by the inflammatory caspases, human caspases 4/5 in human ECs, or the murine homolog caspase-11 in mice in vivo. In caspase-11-deficient mice, BM transplantation with WT hematopoietic cells did not abrogate endotoxemia-induced acute lung injury, indicating a central role for nonhematopoietic caspase-11 in endotoxemia. Additionally, conditional deletion of caspase-11 in ECs reduced endotoxemia-induced lung edema, neutrophil accumulation, and death. These results establish the requisite role of endothelial pyroptosis in endotoxemic tissue injury and suggest that endothelial inflammatory caspases are an important therapeutic target for acute lung injury.
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Citations
Cites
The Acute Respiratory Distress Syndrome
Ware, L. B., & Matthay, M. A. (2000) · New England Journal of Medicine · doi:10.1056/nejm200005043421806 · Cited by 4,666
Caspase-11 cleaves gasdermin D for non-canonical inflammasome signalling
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Inflammasome-activated gasdermin D causes pyroptosis by forming membrane pores
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Pore-forming activity and structural autoinhibition of the gasdermin family
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Non-canonical inflammasome activation targets caspase-11
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Inflammatory caspases are innate immune receptors for intracellular LPS
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Control of adaptive immunity by the innate immune system
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“In a 2-tiered hierarchy of immune surveillance proposed by Iwasaki and Medzhitov (44), the EC should be included not only as an “effector cell” regulating influx of inflammatory cells and fluid and plasma proteins into tissue, but also as a cell capable of sensing intracellular LPS and activating pyroptosis.”
MethodInfluentialThe acute respiratory distress syndrome
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An endogenous caspase-11 ligand elicits interleukin-1 release from living dendritic cells
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“Necroptosislike pyroptosis is a lytic cell death mechanism mediated by kinases such as RIPK3 (27).”
Background
Cited by
Acute respiratory distress syndrome
Matthay, M. A., Zemans, R. L., Zimmerman, G. A., Arabi, Y. M., Beitler, J. R., Mercat, A., Herridge, M., Randolph, A. G., & Calfee, C. S. (2019) · Nature Reviews Disease Primers · doi:10.1038/s41572-019-0069-0 · Cited by 2,387
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Lipid Peroxidation Drives Gasdermin D-Mediated Pyroptosis in Lethal Polymicrobial Sepsis
Kang, R., Zeng, L., Zhu, S., Xie, Y., Liu, J., Wen, Q., Cao, L., Xie, M., Ran, Q., Kroemer, G., et al. (2018) · Cell Host & Microbe · doi:10.1016/j.chom.2018.05.009 · Cited by 608
A 360° view of the inflammasome: Mechanisms of activation, cell death, and diseases
Barnett, K. C., Li, S., Liang, K., & Ting, J. P.-Y. (2023) · Cell · doi:10.1016/j.cell.2023.04.025 · Cited by 458
Huang, L. S., Hong, Z., Wu, W., Xiong, S., Zhong, M., Gao, X., Rehman, J., & Malik, A. B. (2020) · Immunity · doi:10.1016/j.immuni.2020.02.002 · Cited by 435
Self-citation
Metadata
- Authors
- Cheng, K. T., Xiong, S., Ye, Z., Hong, Z., Di, A., Tsang, K. M., Gao, X., An, S., Mittal, M., Vogel, S. M., Miao, E. A., Rehman, J., & Malik, A. B.
- Venue
- Journal of Clinical Investigation
- Published
- 2017-10-09
- Volume
- 127
- Issue
- 11
- Pages
- 4124-4135
- ISSN
- 0021-9738 (ISSN-L)
- 1558-8238
- OpenAlex
- W2763425528
- Cited by
- 471
- References
- 13
- FWCI
- 10.97
- Type
- journal article
- Language
- en
- Open access
- green
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