Phagocyte extracellular traps formation contributes to host defense against Clostridium perfringens infection.

Clostridium perfringens (C. perfringens) is an important Gram-positive anaerobic spore-forming pathogen that provokes life-threatening gas gangrene and acute enterotoxaemia, although it colonizes as a component of the symbiotic bacteria in humans and animals. However, the mechanisms by which C.

G Protein-Coupled Receptor 120 Mediates Host Defense against Infection through Regulating NOD-like Receptor Family Pyrin Domain-Containing 3 Inflammasome Activation.

is a major cause of infectious foodborne disease, frequently associated with the consumption of raw and undercooked food. Despite intensive studies on clarifying pathogenesis, the molecular mechanisms of host-pathogen interactions remain poorly understood. In soft tissue and mucosal infection models, mice, G protein-coupled receptor 120 (GPR120), are more susceptible to infection.

Mixed lineage kinase-like protein protects against infection by enhancing NLRP3 inflammasome-extracellular traps axis.

Despite intense research in understanding () pathogenesis, the mechanisms by which it is cleared from the host are largely unclarified. In gas gangrene and enterocolitis model, mice, lacking mixed lineage kinase-like protein (MLKL), are more susceptible to infection. deficiency results in a defect in inflammasome activation, and IL-18 and IL-1β releases.