Year: 2022

MICROBIAL STRATEGY. "Microbial pathogens may improve their ability to persist in infected hosts by causing the death of cells required for host defense. Although some intracellular pathogens may employ strategies to prevent cell death during pathogen replication, escape and dissemination to new host cells may eventually require cell lysis." https://lnkd.in/eEUp2nB View in LinkedIn

INFLAMMATORY DEATH. "Inflammasome-dependent caspase-1 activity can result in a highly inflammatory form of cell death known as pyroptosis in myeloid cells. Pyroptosis occurs most frequently upon infection with intracellular pathogens and is likely to form part of the antimicrobial response." http://www.sciencedirect.com/science/article/pii/S0092867410000759 View in LinkedIn

MOLECULAR SIGNATURES. "The inflammasome sensor molecules can detect a broad range of molecular signatures to sense microorganisms and tissue stress. They are best known for triggering a robust inflammatory response via the activation of inflammatory caspases." https://lnkd.in/eSuQQy4 View in LinkedIn

NUMEROUS SIGNALS. "Despite their cytosolic location, they are capable of launching an effective immune response against extracellular, vacuolar, and intracellular bacteria, fungi, and viruses. Inflammasomes also sense crystalline substances such as silica and alum, and endogenous danger signals such as ATP, and mount appropriate immune responses." https://lnkd.in/edtaHiu View in LinkedIn

CYTOKINE ACTIVATION. "Inflammasomes are key signalling platforms that detect pathogenic microorganisms and sterile stressors, and that activate the highly pro-inflammatory cytokines interleukin-1β (IL-1β) and IL-18" via caspase activation from cleavage. https://lnkd.in/eSuQQy4 View in LinkedIn

"CASPASES are cysteine proteases that initiate or execute cellular programs, leading to inflammation or cell death. They are synthesized as inactive zymogens, and their potent cellular activities are tightly controlled by proteolytic activation. Caspases are categorized as either proinflammatory or proapoptotic, depending upon their participation in these cellular programs." http://www.sciencedirect.com/science/article/pii/S0092867410000759 View in LinkedIn

DEATH CASCADE. "Formation of inflammasomes in response to microbial or danger signals leads to cleavage of procaspase-1 into active caspase-1 enzyme, which further cleaves proforms of the inflammatory cytokines, IL-1β and IL-18, into their active forms. Inflammasome activation also results in pyroptosis, an inflammatory form of cell death." https://lnkd.in/edtaHiu View in LinkedIn

EXTRACELLULAR ATP. "It is well known that the extracellular ATP concentration is negligible in healthy tissues (in the low nanomolar range), but it is equally well known that the extracellular ATP levels may rise to the high micromolar level following tissue damage at sites of inflammation or within the tumor microenvironment." https://lnkd.in/eNNPn5D View in LinkedIn

ATP ALARM SIGNAL "ATP itself is a very efficient extracellular distress signal because, with the extracellular level normally very low, even minute leaks can increase the pericellular concentration several fold." https://lnkd.in/eNNPn5D View in LinkedIn

ATP RECEPTOR. "This receptor has a special place in inflammasome biology because its stimulation is still used as one of the most potent and reliable means to activate the NLRP3 inflammasome. The P2X7R is ideally suited to respond to unusual, pathologic ATP tissue levels because of its very high EC50 for ATP (between 100 and 300 μM) and lack of desensitization. These features allow P2X7R to open most frequently when extracellular ATP is elevated above physiologic levels." https://lnkd.in/eNNPn5D View in LinkedIn