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Impact of Nutrition and Dietary Supplementation on Psoriasis Pathology
Published in Siba P. Raychaudhuri, Smriti K. Raychaudhuri, Debasis Bagchi, Psoriasis and Psoriatic Arthritis, 2017
Odete Mendes, Mithila Shitut, Jayson Chen
The therapeutic effects of mustard seed (Sinapis alba Linn) were investigated for the role of NLRP3 inflammasome in IMQ-induced psoriasis-like inflammation in mice (Hu et al., 2013; Jiang et al., 2015). Mustard seed attenuated the inductions of NLRP3, ASC, caspase-1, and caspase-11 mRNA expressions; ASC and caspase-1 protein expressions; and serum levels of IL-1β and IL-18 caused by IMQ treatment. These results suggest that mustard seed can suppress inflammation induced by IL-1β and IL-18 by downregulating the expression of NLRP3 inflammasome.
The Role of Nanoparticles in Cancer Therapy through Apoptosis Induction
Published in Hala Gali-Muhtasib, Racha Chouaib, Nanoparticle Drug Delivery Systems for Cancer Treatment, 2020
Marveh Rahmati, Saeid Amanpour, Hadiseh Mohammadpour
Apoptosis is an energy-dependent process. Two main apoptotic signaling pathways, including the extrinsic death receptor pathway and the intrinsic mitochondrial pathway, have been well-characterized. However, there are additional pathways that involve the T-cell-mediated cytotoxicity and the perforin-granzyme pathway. The perforin/granzyme pathway induces apoptosis through either granzyme B or granzyme A. Another recent pathway of apoptosis is mediated by the endoplasmic reticulum (ER) which plays important roles in cell fate and will be discussed in details later [17]. Apoptosis is mediated by chronological activation of protein superfamily of caspases [16]. Caspases are expressed in an inactive form of proenzymes in most cells. When activated, they activate other procaspases, leading to the initiation of the cascade of caspase-dependent apoptosis pathway. Caspases are highly conserved cysteine-dependent aspartate-specific proteases. There are different types of caspases: initiator caspases, including CASP-2, 8, 9, and 10; effector caspases, such as CASP-3, 6, and 7; and inflammatory caspases which are CASP-1, 4, and 5). The other caspases that have been recently studied are (i) caspase-11, which is involved in the regulation of apoptosis and cytokine maturation during septic shock, (ii) caspase-12, which mediates apoptosis through the endoplasmic reticulum, (iii) caspase-13, which is believed to be a bovine gene, and (iv) caspase-14, which is highly expressed just in embryonic tissues [23]. Initiator caspases are inactive until specific oligomeric activator protein binds to them. Subsequently, they bind to effector caspases. Effector caspases are then activated through proteolytic cleavage. The activated caspases then proteolytically degrade the intracellular proteins necessary for programmed cell death.
Pyroptosis in neurodegenerative diseases: What lies beneath the tip of the iceberg?
Published in International Reviews of Immunology, 2023
Mengli Yue, Li Xiao, Rui Yan, Xinyi Li, Wei Yang
Cpb1-C3-C3aR participates in the regulation of pyroptosis by enhancing the expression of caspase-11 through positive feedback. C3aR contributes to Caspase11/GSDMD-mediated cell pyroptosis. When TLR4 and IFN-α receptor on the cell surface are activated by their respective ligands, proinflammatory genes such as TNF, IL-6, caspase11 and C3 are induced to express through various mechanisms including MAPK/P38. In macrophages, C3 is cleaved into C3a and C3b and quickly released into extracellular. Cpb1 cleaves C3a to form C3a-desArg, which bind and activate C3aR on the cell membrane and then enhances the downstream MAPK/p38 activity, by promoting the phosphorylation of MAPK. This will positively regulate the expression of inflammatory mediators such as caspase-11. Caspase-11, when gets released, is able to activate TLR4 and IFN-α receptor on the cell surface in feedback [84].
Genetic and Epigenetic Regulation of the Innate Immune Response to Gout
Published in Immunological Investigations, 2023
Jordana Dinorá de Lima, André Guilherme Portela de Paula, Bruna Sadae Yuasa, Caio Cesar de Souza Smanioto, Maria Clara da Cruz Silva, Priscila Ianzen dos Santos, Karin Braun Prado, Angelica Beate Winter Boldt, Tárcio Teodoro Braga
On the other hand, neutrophils may clear the joint by releasing neutrophil extracellular traps (NETs) through the mixed lineage kinase domain-like (MLKL) pathway (Garcia-Gonzalez et al. 2021), easing MSU macrophage digestion (Jeong et al. 2021). NET release, also called NETosis, depends more on the number of crystals than of infiltrated cells (Garcia-Gonzalez et al. 2021). Thus, chronic tophaceous gout is characterized by higher NETosis, due to the higher number of crystals. Molecularly, Caspase-11 promotes neutrophil chemotaxis and NET formation (Caution et al. 2019). Also, NET formation can also be activated by nuclear-factor, interleukin 3 regulated protein (NFIL3)/regulated in development and DNA damage response 1 (REDD1)/mechanistic target of rapamycin (mTOR) axis, which activates autophagy in parallel (Tang et al. 2021). Neutrophils ultimately reduce inflammation by activating spleen tyrosine (Syk) and phosphatidyl inositol 3 (PI3-K) kinases (Cunningham et al. 2012).
Inhibition of Caspase-11-Mediated Pyroptosis Alleviates Acute Kidney Injury Associated with Severe Acute Pancreatitis in Rats
Published in Journal of Investigative Surgery, 2023
Yang Shao, Chang Li, Yingjian Jiang, Hongbo Li, Xuefei Tang, Zhaoyu Gao, Dianliang Zhang
Pyroptosis is essentially an intrinsic immune reaction and contributes to the clearance of exogenous invasion by causing local inflammatory reactions [20]. However, severe pyroptosis may lead to an uncontrolled local inflammatory reaction, which may cause tissue damage and even organ failure. Caspase-11 can trigger the non-canonical pyroptosis pathway when activated by lipopolysaccharide [22]. Recent studies have proved that caspase-11-mediated pyroptosis involves cisplatin, contrast, or sepsis-induced renal injury [14, 15, 23]. A significant increase in caspase-11 and caspase-11 P20 protein in the renal tissue of the SAP rat model was observed in the current study. GSDMD, a crucial downstream target of caspase-11, is involved in pyroptosis and causes rapid lytic cell death by promoting cell pore formation [24]. Here, we also observed the upregulation of GSDMD as well as GSDMD-N expressions in the renal tissue of SAP rats. In summary, these observations revealed that caspase-11-mediated pyroptosis occurs in the renal injury induced by SAP. Furthermore, it is hypothesized that pyroptosis occurs mostly in renal tubular epithelia because GSDMD and caspase-11 were highly expressed in renal tubular epithelia.