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Published on: September 20, 2018
Inflammatory caspase-related pyroptosis: mechanism, regulation and therapeutic potential for inflammatory bowel
Yuan-Yuan Yuan1, Ke-Xin Xie2, Sha-Long Wang1
1Department of Geriatric Surgery, The Second Xiangya Hospital of Central South University, Changsha, Hunan 410011, China.
Abstract:
As an essential part of programmed cell death, pyroptosis is an inflammatory response that is elicited upon infection by intracellular pathogens. Metabolic diseases, atherosclerosis and vital organ damage occur if pyroptosis is over-activated. Macrophages are the main cells that induce pyroptosis with the help of intracellular pattern-recognition receptors stimulated by danger signals and pathogenic microorganisms in the cytosol of host cells. Activated inflammatory caspases induce pyroptosis and produce pro-inflammatory cytokines, such as interleukin-1β and interleukin-18. Inflammatory programmed cell death is classified as canonical or non-canonical based on inflammatory caspases, which includes caspase-1 (in human and mouse) and caspase-11 (in mouse) or caspase-4 and -5 (in humans). Activated inflammatory caspases cleave the pore-forming effector protein, gasdermin-D, inducing osmotic pressure deregulation of internal fluids and subsequently rupturing the cell membranes. Inflammatory caspases could be attractive therapeutic targets for inflammatory bowel disease (IBD) in which pyroptosis may play an important role. This article reviews the current understanding of the mechanism of pyroptosis, focusing on the regulation of inflammatory caspases and therapeutic strategies for IBD.
Insights
Pyroptosis is an inflammatory cell death crucial for fighting pathogens but harmful when overactive. Targeting inflammatory caspases offers potential therapies for inflammatory bowel disease (IBD).
Area of Science:
- Immunology
- Cell Biology
- Pathology
Background:
- Pyroptosis is a programmed inflammatory cell death, essential for combating intracellular pathogens.
- Overactivation of pyroptosis contributes to metabolic diseases, atherosclerosis, and organ damage.
Purpose of the Study:
- To review the mechanism of pyroptosis, emphasizing inflammatory caspase regulation.
- To explore therapeutic strategies for inflammatory bowel disease (IBD) targeting pyroptosis.
Main Methods:
- Review of current literature on pyroptosis mechanisms.
- Focus on inflammatory caspases (caspase-1, -11, -4, -5) and gasdermin-D.
- Analysis of pyroptosis's role in inflammatory bowel disease (IBD).
Main Results:
- Pyroptosis is initiated by intracellular pattern-recognition receptors sensing danger signals.
- Activated inflammatory caspases cleave gasdermin-D, leading to cell membrane rupture.
- Interleukin-1β and interleukin-18 are key pro-inflammatory cytokines produced during pyroptosis.
Conclusions:
- Inflammatory caspases are central regulators of pyroptosis.
- Targeting inflammatory caspases presents a promising therapeutic avenue for IBD.
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