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IL-1 Receptor Antagonist Ameliorates Inflammasome-Dependent Inflammation in Murine and Human Cystic Fibrosis

IL-1 Receptor Antagonist Ameliorates Inflammasome-Dependent Inflammation in Murine and Human Cystic Fibrosis

Rossana G Iannitti, Valerio Napolioni, Vasilis Oikonomou, Antonella De Luca, Claudia Galosi, Marilena Pariano, Cristina Massi-Benedetti, Monica Borghi, Matteo Puccetti, Vincenzina Lucidi, Carla Colombo, etc.

Nat Commun. 2016 Mar 14;7:10791.

PMID: 26972847

Abstract:

Dysregulated inflammasome activation contributes to respiratory infections and pathologic airway inflammation. Through basic and translational approaches involving murine models and human genetic epidemiology, we show here the importance of the different inflammasomes in regulating inflammatory responses in mice and humans with cystic fibrosis (CF), a life-threatening disorder of the lungs and digestive system. While both contributing to pathogen clearance, NLRP3 more than NLRC4 contributes to deleterious inflammatory responses in CF and correlates with defective NLRC4-dependent IL-1Ra production. Disease susceptibility in mice and microbial colonization in humans occurs in conditions of genetic deficiency of NLRC4 or IL-1Ra and can be rescued by administration of the recombinant IL-1Ra, anakinra. These results indicate that pathogenic NLRP3 activity in CF could be negatively regulated by IL-1Ra and provide a proof-of-concept evidence that inflammasomes are potential targets to limit the pathological consequences of microbial colonization in CF.

Chemicals Related in the Paper:

Catalog Number	Product Name	Structure	CAS Number	Price
IAR42413332	IL-1RA murine			Price

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