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NLRP3 deficiency abrogates silica-induced neutrophil infiltration, pulmonary damage and fibrosis - Respiratory Research
References Lam M, Mansell A, Tate MD. Another One Fights the Dust: Targeting the NLRP3 Inflammasome for the Treatment of Silicosis. Am J Respir Cell Mol Biol. 2022;66:601–11. Hoy RF, Jeebhay MF, Cavalin C, Chen W, Cohen RA, Fireman E, et al. Current global perspectives on silicosis—Convergence of old and newly emergent hazards. Respirology. 2022;27:387–98. Merlo DF, Garattini S, Gelatti U, Simonati C, Covolo L, Ceppi M, et al.
NLRP1B allele 2 does not respond to Val-boro-Pro (VbP) in the intestinal epithelium
Abstract The intestinal mucosa must balance tolerance to commensal microbes and luminal antigens with rapid detection of enteric pathogens in order to maintain homeostasis. This balance is facilitated through the regulation of epithelial layer integrity by innate immune receptors. Certain NOD-like receptors (NLRs) expressed in intestinal epithelial cells, including NLRC4 and NLRP9B, form inflammasomes that protect against pathogens by activating caspase-1 to cause extrusion of infected cells.
Helminth infection driven gastrointestinal hypermotility is independent of eosinophils and mediated by alterations in smooth muscle instead of enteric neurons
Abstract Intestinal helminth infection triggers a type 2 immune response that promotes a weep-and sweep response characterised by increased mucus secretion and intestinal hypermotility, which function to dislodge the worm from its intestinal habitat. Recent studies have discovered that several other pathogens cause intestinal dysmotility through major alterations to the immune and enteric nervous systems (ENS), and their interactions, within the gastrointestinal tract.
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