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Abstract Cryopyrin-associated periodic syndromes (CAPS) are autoinflammatory disorders caused by gain-of-function NLRP3 variants. Although NLRP3 inflammasomes mediate IL-1β secretion through Gasdermin D (GSDMD), we show that GSDMD deletion did not prevent autoinflammation in mice ubiquitously expressing the Nlrp3A350V variant. Inflamed skin of Nlrp3A350V-expressing GSDMD-deficient mice displayed citrullinated histone 3-containing neutrophil extracellular traps (CitH3-NETs).
1 Introduction Interleukin (IL)-1β is a key inflammatory cytokine that has a broad activity causing fever, inducing acute-phase proteins, and recruiting and activating immune cells (1). IL-1β can be released in response to infection but has also been associated with the pathogenesis of many sterile inflammatory diseases, including gout, type 2 diabetes and rheumatoid arthritis (1–3).
1 Introduction Pyroptosis is a form of regulated cell death that depends on the formation of plasma membrane pores by members of the gasdermin (GSDM) protein family, often due to inflammatory caspase activation (Galluzzi et al., 2018). In the 1990s, pyroptosis was initially described as a caspase-1-dependent and bacteria-induced necrotic cell death; present in macrophages infected with Salmonella typhimurium (Zychlinsky et al., 1992; Monack et al., 1996).
Commensal microbial communities play critical roles in shaping human health. A substantial body of scientific and clinical evidence links microbial dysbiosis to inflammatory bowel diseases, metabolic disease, and numerous other diseases that affect humanity. One of the challenges ahead in realizing the full biomedical potential of microbiome modulation lies in defining the host and environmental factors and mechanisms that modulate the microbiota composition.
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