About this Research Topic

Manuscript Submission Deadline 22 September 2022
Manuscript Extension Submission Deadline 22 October 2022

Microbial infections and damage to host cells can activate inflammasomes, which mediate tissue inflammation and adaptive immunity. Inflammasomes are innate immune mechanisms that promote inflammation by activating caspase-1 protease and are associated with cell death, such as pyroptosis and apoptosis. ...

Microbial infections and damage to host cells can activate inflammasomes, which mediate tissue inflammation and adaptive immunity. Inflammasomes are innate immune mechanisms that promote inflammation by activating caspase-1 protease and are associated with cell death, such as pyroptosis and apoptosis. Although inflammasome and IL-1β signaling are crucial in tissue inflammation, little was known about their regulatory mechanism. Inflammasome activation and subsequent pyroptosis are critical defense mechanisms against pathogenic microorganisms. However, overactivation of the inflammasome leads to the death of the host. Activation of the inflammasome by Gram-negative bacteria or non-canonical activation of the inflammasome by lipopolysaccharide (LPS) can induce systemic blood clotting and massive tissue thrombosis. Furthermore, the production of reactive oxygen species and lysosomal damage have been shown to trigger the inflammasome. Additionally, inflammasome-activated cells undergo inflammatory cell death associated with the release of potent pro-inflammatory cytokines and extracellular vesicles (EVs) have been poorly characterized.

Inflammasome-induced extracellular vesicles (EVs) can serve as biomarkers for inflammasome activation and act in the prevention of systemic hyperinflammatory states by restricting NLRP3 activation in eukaryotic cells. The NLRP3 nflammasome is activated by diverse stimuli and multiple molecular and cellular events, including infections by microorganisms, production of reactive oxygen species, and lysosomal damage. However, the signaling and assembly events of the inflammasome is not fully understood. Inflammasomes can cause mitochondrial fission with the release of microvesicles into host cells, resulting in disordered function in capillaries and venules. Therefore, inflammasomes may contribute to the pathogenesis of inflammatory disorders and host defenses against microbial pathogens. Understanding the molecular mechanisms of inflammasome-associated cell death and its physiological implications may contribute to the development of new therapeutic strategies for inflammasome-related infectious diseases.

In this research topic, we welcome Original Research articles, Mini Reviews, Reviews, and Perspective articles covering inflammasome activation by microorganisms and extracellular vesicles:

• Microbiota and host Inflammasome
• Inflammasome activation by microorganisms
• Inflammasome, inflammation, and tissue homeostasis
• Inflammasome as sensor of pathogens and cellular perturbations
• Inflammasomes, autophagy, and cell death against microorganisms
• Pyroptosis in macrophages stimulated by human pathogens
• NLRP3 inflammasome activation by pathogens extracellular vesicles
• NLRP3 Inflammasome and its role in sepsis development by pathogens
• Membrane vesicles from pathogens and activation of inflammasome through caspases in human cells
• ROS and inflammasome activation by microorganisms
• Detection of bacterial membrane vesicles by NOD-like receptors
• Extracellular vesicles from microorganisms and capacity to elicit host immune response
• Molecular mechanisms and functions of pyroptosis, inflammatory caspases, and inflammasomes in infectious diseases.

Keywords: Inflammasomes, infectious diseases, pyroptosis and apoptosis, extracellular vesicles, reactive oxygen species


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