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© Charles DAUGUET, Institut Pasteur
HIV particles
Publication : Journal of immunology (Baltimore, Md. : 1950)

IL-1R1/MyD88 signaling is critical for elastase-induced lung inflammation and emphysema

Scientific Fields
Diseases
Organisms
Applications
Technique

Published in Journal of immunology (Baltimore, Md. : 1950) - 15 Dec 2009

Couillin I, Vasseur V, Charron S, Gasse P, Tavernier M, Guillet J, Lagente V, Fick L, Jacobs M, Coelho FR, Moser R, Ryffel B

Link to Pubmed [PMID] – 20007584

J. Immunol. 2009 Dec;183(12):8195-202

Lung emphysema and fibrosis are severe complications of chronic obstructive pulmonary disease, and uncontrolled protease activation may be involved in the pathogenesis. Using experimental elastase-induced acute inflammation, we demonstrate here that inflammation and development of emphysema is IL-1R1 and Toll/IL-1R signal transduction adaptor MyD88 dependent; however, TLR recognition is dispensable in this model. Elastase induces IL-1beta, TNF-alpha, keratinocyte-derived chemokine, and IL-6 secretion and neutrophil recruitment in the lung, which is drastically reduced in the absence of IL-1R1 or MyD88. Further, tissue destruction with emphysema and fibrosis is attenuated in the lungs of IL-1R1- and MyD88-deficient mice. Specific blockade of IL-1 by IL-1R antagonist diminishes acute inflammation and emphysema. Finally, IL-1beta production and inflammation are reduced in mice deficient for the NALP3 inflammasome component apoptosis-associated speck-like protein containing a caspase recruitment domain (ASC), and we identified uric acid, which is produced upon elastase-induced lung injury, as an activator of the NALP3/ASC inflammasome. In conclusion, elastase-mediated lung pathology depends on inflammasome activation with IL-1beta production. IL-1beta therefore represents a critical mediator and a possible therapeutic target of lung inflammation leading to emphysema.

http://www.ncbi.nlm.nih.gov/pubmed/20007584