The NOD-like receptor protein 3 (NLRP3) inflammasome is a protein complex that regulates innate immune responses by activating caspase-1 and the inflammatory cytokines interleukin (IL)-1β and IL-18. Multiple studies have demonstrated the importance of the NLRP3 inflammasome in the development of immune and inflammation-related diseases, including arthritis, Alzheimer's disease, inflammatory bowel disease, and other autoimmune and autoinflammatory diseases. This review first explains the activation and regulatory mechanism of the NLRP3 inflammasome. Secondly, we focus on the role of the NLRP3 inflammasome in various inflammation-related diseases. Finally, we look forward to new methods for targeting the NLRP3 inflammasome to treat inflammation-related diseases, and provide new ideas for clinical treatment. 

/pdf/the-nlrp3-inflammasome-contributions-to-inflammation-related-3p24dk6j.pdf

The NLRP3 inflammasome: contributions to inflammation-related diseases

Autoimmune diseases (AIDs) emerge due to an irregular immune response towards self- and non-self-antigens. Inflammation commonly accompanies these conditions, with inflammatory factors and inflammasomes playing pivotal roles in their progression. Key concepts in molecular biology, inflammation, and molecular mimicry are crucial to understanding AID development. Exposure to foreign antigens can cause inflammation, potentially leading to AIDs through molecular mimicry triggered by cross-reactive epitopes. Molecular mimicry emerges as a key mechanism by which infectious or chemical agents trigger autoimmunity. In certain susceptible individuals, autoreactive T or B cells may be activated by a foreign antigen due to resemblances between foreign and self-peptides. Chronic inflammation, typically driven by abnormal immune responses, is strongly associated with AID pathogenesis. Inflammasomes, which are vital cytosolic multiprotein complexes assembled in response to infections and stress, are crucial to activating inflammatory processes in macrophages. Chronic inflammation, characterized by prolonged tissue injury and repair cycles, can significantly damage tissues, thereby increasing the risk of AIDs. Inhibiting inflammasomes, particularly in autoinflammatory disorders, has garnered significant interest, with pharmaceutical advancements targeting cytokines and inflammasomes showing promise in AID management.

Inflammasome Molecular Insights in Autoimmune Diseases

Abdominal aortic aneurysm (AAA) has been recognized as a serious chronic inflammatory degenerative aortic disease in recent years. At present, there is no other effective intervention except surgical treatment for AAA. With the aging of the human population, its incidence is increasing year by year, posing a serious threat to human health. Modern studies suggest that vascular chronic inflammatory response is the core process in AAA occurrence and development. Inflammasome, a multiprotein complex located in the cytoplasm, mediates the expression of various inflammatory cytokines like interleukin (IL)-1β and IL-18, and thus plays a pivotal role in inflammation regulation. Therefore, inflammasome may exert a crucial influence on the progression of AAA. This article reviews some mechanism studies to investigate the role of inflammasome in AAA and then summarizes several potential drugs targeting inflammasome for the treatment of AAA, aiming to provide new ideas for the clinical prevention and treatment of AAA beyond surgical methods.

The Role of Inflammasome in Abdominal Aortic Aneurysm and Its Potential Drugs

Sepsis, a systemic inflammatory response triggered by infection, has a considerably high mortality rate. However, effective prevention and intervention measures against sepsis remain insufficient. Therefore, this study aimed to investigate the mechanisms underlying the protective properties of immune response gene-1 (IRG1) and 4-Octyl itaconate (OI) during acute liver damage in mice with sepsis. A sepsis mouse model was established to compare wild-type and IRG1-/- groups. The impact of IRG1/Itaconate on pro- and anti-inflammatory cytokines was evaluated using J774A.1 cells. IRG1/Itaconate substantially reduced pro-inflammatory cytokines and increased the release of anti-inflammatory cytokines. It reduced pathological damage to liver tissues, preserved normal liver function, decreased the release of reactive oxygen species (ROS) and LDH, and enhanced the GSH/GSSG ratio. Moreover, IRG1 and itaconic acid activated the Nrf2 signaling pathway, regulating the expression of its downstream antioxidative stress-related proteins. Additionally, they inhibited the activity of NLRP3 inflammatory vesicles to suppress the expression of macrophage-associated pyroptosis signaling molecules. Our findings demonstrate that IRG1/OI inhibits NLRP3 inflammatory vesicle activation and macrophage pyroptosis by modulating the Nrf2 signaling pathway, thereby attenuating acute liver injury in mice with sepsis. These findings could facilitate the clinical application of IRG1/Itaconate to prevent sepsis-induced acute liver injury. 

IRG1/itaconate alleviates acute liver injury in septic mice by suppressing NLRP3 expression and its mediated macrophage pyroptosis via regulation of the Nrf2 pathway.

We previously found that acrylamide (AA) damaged RAW264.7 cells (a kind of macrophages) by up-regulating P2X7 protein level, and Yam polysaccharides (YPS) could protect RAW264.7 cells against AA injury. Macrophages polarization may generate various subtypes which are closely related with cell function. However, how AA and YPS influence RAW264.7 polarization is unknown. In this study, we studied the effects of AA and YPS on the polarization of RAW264.7 cells. The killing effect of RAW264.7 cell on tumor cells has also been evaluated. The results showed that AA caused cell polarization towards M1-like macrophages by elevating CD86 and COX-2 protein expression and decreasing CD206 protein expression. Inhibiting the expression of P2X7 protein could effectively interfere with AA-induced M1 polarization. YPS could modulate AA-induced M1 polarization by reducing the ratio of CD86/CD206 but not COX-2 protein expression. RAW264.7 cell medium treated with AA had no effect on HepG2 cancer cell viability, but RAW264.7 cell medium treated with YPS significantly inhibited HepG2 cell viability. These findings suggested that YPS could regulate AA-induced RAW264.7 polarization and improve cell function. The results will provide reference for further explaining the mechanism of YPS intervening in toxic AA. 

pdf/the-effects-of-yam-polysaccharides-on-acrylamide-induced-4rc97d62pk.pdf

The effects of Yam polysaccharides on acrylamide-induced RAW264.7 cell polarization

Purinergic Receptor P2 × 7 Contributes to Abdominal Aortic Aneurysm Development via Modulating Macrophage Pyroptosis and Inflammation.

Hirudin ameliorates myocardial ischemia-reperfusion injury in a rat model of hemorrhagic shock and resuscitation: roles of NLRP3-signaling pathway.

Bibliometric analysis of the top 100 most-cited articles on branch reconstruction in endovascular aortic repair.

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Purinergic Receptor P2 × 7 Contributes to Abdominal Aortic Aneurysm Development via Modulating Macrophage Pyroptosis and Inflammation.

Hirudin ameliorates myocardial ischemia-reperfusion injury in a rat model of hemorrhagic shock and resuscitation: roles of NLRP3-signaling pathway.

Bibliometric analysis of the top 100 most-cited articles on branch reconstruction in endovascular aortic repair.

Peng Lu

Author Tools

Chat about Author

Papers

Purinergic Receptor P2 × 7 Contributes to Abdominal Aortic Aneurysm Development via Modulating Macrophage Pyroptosis and Inflammation.

Hirudin ameliorates myocardial ischemia-reperfusion injury in a rat model of hemorrhagic shock and resuscitation: roles of NLRP3-signaling pathway.

Bibliometric analysis of the top 100 most-cited articles on branch reconstruction in endovascular aortic repair.

Purinergic Receptor P2 × 7 Contributes to Abdominal Aortic Aneurysm Development via Modulating Macrophage Pyroptosis and Inflammation.