NLRP3 (NLR Family Pyrin Domain Containing 3)

GSDMD immunostaining detected pericellular pores forming around the membrane of NFTs and in NPs. Messenger RNA and protein analyses demonstrate that inflammasome signaling molecules are elevated in AD suggesting that neuronal death occurs by the induction of pyroptosis.

At the same time, A. muciniphila administration improves cognitive deficits, alleviates neuroinflammation and Aβ deposition via AhR/NF-κB/NLRP3 signaling pathway in APP/PS1 mice. In summary, our findings suggest A. muciniphila is a promising approach for preventing AD progression by microbiota-gut-brain axis.

We further discuss emerging evidence linking CBD's regulation in the gut to systemic effects along the gut-organ axis, including the gut-brain and gut-liver axes. Overall, this review synthesizes current evidence on how CBD integrates redox modulation, inflammation control, and intestinal barrier protection, providing a mechanistic framework for its potential application in intestinal disease and health.

Consistent with the in vivo results, the NF-κB/NLRP3 pathway and the secretion of inflammatory cytokines were inhibited after SNX10 knockdown in A549 cells. In summary, SNX10 downregulation mitigated sepsis-induced oxidative stress and pulmonary inflammation by inhibiting the NF-κB/NLRP3 pathway.

Furthermore, E171-induced secretion of S100A8 and S100A9 in macrophages was suppressed by specific inhibitors, including N-acetylcysteine (NAC, ROS inhibitor), MCC950 (NLRP3 inhibitor), Z-YVAD-FMK (caspase 1 inhibitor), disulfiram (GSDMD inhibitor), and transfection of NLRP3 small interfering ribonucleic acid (siRNA). These results indicate that dietary E171 promotes CAC development by activating macrophages, with S100A8 and S100A9 serving as key mediators, and the NLRP3/caspase 1/GSDMD pathway acting as a critical mechanism.

Our findings indicate that Grg3 confers protective effects in a murine model of imiquimod-induced psoriasis-like dermatitis. The potential therapeutic properties of Grg3 potentially involve modulation of NLRP3 inflammasome activation, suppression of NF-κB signaling, and restoration of Th17/Treg cell homeostasis.

The anti-tumor immunity is abrogated by caspase-1 inhibitor VX-765, anti-IL-1β, and anti-IL-18...Finally, Tmem175-/- mice are more responsive to anti-PD-1. Our works implies TMEM175 to be a potential target for immunotherapy.

This study provides an NSCLC-specific transcriptional framework linking NFκB activity to autophagy- and inflammation-associated gene networks. By integrating expression profiling and in silico analyses, we identify candidate NFκB-responsive genes, including NLRP3, that may contribute to autophagy-related cellular responses in NSCLC.

Compounds S2-4 (0.58 ± 0.07 μM) and S2-8 (0.42 ± 0.04 μM) demonstrated the greatest potency towards H838 cells; compounds S2-13 (1.28 ± 0.13 μM) and S2-14 (1.80 ± 0.24 μM) exhibited potent and selective activity towards H838 cells. Molecular docking studies of S2-4/NLRP3 and S2-14/STAT3, combined with the structure-activity relationship (SAR) analysis, indicated that the benzofuran core containing an ortho-quinone, along with an amide linkage and a 1,2,3-triazole group introduced at the C-2 position of the furan ring, is an effective chemical scaffold for enhancing the anti-NSCLC activity of tanshinone derivatives.

Furthermore, in muscle cells, MCC950 directly silences NLRP3 inflammasome signaling, inhibits pyroptosis and IL-1β/IL-18 secretion, suppresses muscle protein degradation to rescue cancer cachexia-driven muscle atrophy. These findings revealed the important role of NLRP3 inflammasome in cancer cachexia and also suggested the possibility of developing NLRP3 inflammasome inhibitors such as MCC950 to be novel therapeutic candidates for cancer cachexia treatment.

In addition, suppressing or overexpressing METTL3, YTHDF1, and NMDAR2B correspondingly decreased or increased these effects, but modulation of NMDAR2B did not change the expression of METTL3/YTHDF1. rTMS can affect the polarization state of microglia and neuroinflammation by regulating the METTL3/NMDAR2B/NLRP3 signaling pathway, thereby improving NeuP.

TAFA4 acts as a neuron-derived mediator of neuroimmune crosstalk in IVDD that modulates macrophage polarization and oxidative stress, thereby delaying disc degeneration. This neuron-immune axis represents a potential therapeutic target.