A5101941765- Inflammasome and immune disorders
- Heme Oxygenase-1 and Carbon Monoxide
- Erythrocyte Function and Pathophysiology
- Toxoplasma gondii Research Studies
- Streptococcal Infections and Treatments
- Marine Invertebrate Physiology and Ecology
- Bacterial Infections and Vaccines
- Biomarkers in Disease Mechanisms
- Amoebic Infections and Treatments
- interferon and immune responses
- Trace Elements in Health
- Immune Response and Inflammation
- Ferroptosis and cancer prognosis
- IL-33, ST2, and ILC Pathways
East China University of Science and Technology
2018-2024
The noncanonical inflammasome is critical for cytosolic sensing of Gram-negative pathogens. Here, we show that bacterial infection induces caspy2 activation in zebrafish fibroblasts, which mediates pyroptosis via a caspase-5-like activity. Zebrafish binds directly to lipopolysaccharide the N-terminal pyrin death domain, resulting oligomerization, pyroptosis. Furthermore, highly expressed gut and activated during infection. Knockdown expression impairs ability restrict invasion vivo, protects...
Inflammatory caspase-11/4/5 recognize cytosolic LPS from invading Gram-negative bacteria and induce pyroptosis cytokine release, forming rapid innate antibacterial defenses. Since extracellular or vacuole-constrained are thought to rarely access the cytoplasm, how their exposed sensors is a critical event for pathogen recognition. Hemolysin pore-forming bacterial toxin, which was generally accepted rupture cell membrane, leading lysis. Whether hemolysin participates in non-canonical...
Inflammatory caspases sensing lipopolysaccharide (LPS) to drive gasdermin (GSDM)–mediated pyroptosis is an important immune response mechanism for anti-infection defense in mammals. In this work, we resolved LPS-induced and GSDM-gated signaling cascade Cnidarians. Initially, identified a functional GSDM protein, HyGSDME, Hydra , executing cytosolic caspase-dependent manner. Further, proinflammatory caspase, HyCaspA capable of LPS by uncharacterized N-terminal domain relying on its unique...
Mesenchymal stromal cells (MSCs) based therapy is a promising approach to treat inflammatory disorders. However, therapeutic effect not always achieved. Thus the mechanism involved in inflammation requires further elucidation. To explore mechanisms by which MSCs respond stimuli, we investigated whether employed inflammasomes participate inflammation. Using vitro and vivo models, found that canonical NLRP3 non-canonical caspase-11 were activated bone-associated (BA-MSCs) promote response. The...
Programmed cell death plays an important role in modulating host immune defense and pathogen infection. Ferroptosis is a type of inflammatory induced by intracellular iron-dependent accumulation toxic lipid peroxides. Although ferroptosis has been associated with cancer other sterile diseases, very little known about the host-pathogen interactions. We show that secondary messenger bis-(3′,5′)-cyclic dimeric GMP (c-di-GMP) pathogenic bacterium Edwardsiella piscicida ( E. ) triggers...
Inflammasomes are important innate immune components in mammals. However, the bacterial factors modulating inflammasome activation fish, and mechanisms by which they alter fish defences, remain to be investigated. In this work, a mutant of pathogen Edwardsiella piscicida (E. piscicida), called 0909I, was shown overexpress haemolysin, could induce robust pyroptotic-like cell death dependent on caspase-5-like activity during infection nonphagocyte cells. E. haemolysin found mainly associate...
Abstract Inflammatory caspase-11/4/5 recognize cytosolic LPS from invading Gram-negative bacteria and induce pyroptosis cytokine release, forming rapid innate antibacterial defenses. Since extracellular or vacuole-constrained are thought to rarely access the cytoplasm, how their exposed sensors is a critical event for pathogen recognition. Hemolysin pore-forming bacterial toxin, which was generally accepted rupture cell membrane, leading lysis. Whether hemolysin participates in non-canonical...
The canonical complement-mediated lysis of red blood cells (RBCs) leads to serious pathogenesis. However, inhibition strategies targeting complements are not always as efficient expected in the clinical setting. To seek for more therapy, we investigated intracellular events RBCs following complement activation, which had been neglected a long time. Here, demonstrated that complement-induced hemolysis was caspase-8-dependent programmed RBC death. Furthermore, short NLRP3 (miniNLRP3) fragments...