Inflammasomes in the lung. (June 2017)

• Record Type: Journal Article
• Authors: Pinkerton, James W.; Kim, Richard Y.; Robertson, Avril A.B.; Hirota, Jeremy A.; Wood, Lisa G.; Knight, Darryl A.; Cooper, Matthew A.; O'Neill, Luke A.J.; Horvat, Jay C.; Hansbro, Philip M.
• Is Part Of: Molecular immunology. Volume 86(2017:Jun.)
• Page Start: 44
• Page End: 55
• Publication Date: 2017-06
• Subjects: AAD allergic airways disease -- AHR airways hyperresponsiveness -- AIM absent in melanoma -- ALI acute lung injury -- Alum aluminium hydroxide -- ARDS acute respiratory distress syndrome -- BALF bronchoalveolar lavage fluid -- CAP community acquired pneumonia -- CAPS cryopyrin-associated periodic syndrome -- Casp1 Caspase-1 -- CARD caspase-recruitment domain -- CF cystic fibrosis -- CFTR CF transmembrane conductance regulator -- COPD chronic obstructive pulmonary disease -- DAMP damage-associated molecular patterns -- HDM house dust mite -- HIN haemopoietic IFN-inducible nuclear -- HMGB1 chromatin-binding high motility group box 1 protein -- IAV influenza A virus -- LRR C-terminal leucine rich repeats -- NBD nucleotide binding domain -- NLR NOD-like receptor -- NOD nucleotide oligomerisation domain -- NLRC NOD-like receptor containing -- NLRP NOD-like receptor protein -- Ova ovalbumin -- PAMP pathogen-associated molecular pattern -- PRR pattern recognition receptor -- PYD pyrin domain -- PYHIN pyrin and haemopoietic IFN-inducible nuclear -- ROS reactive oxygen species -- SSI severe, steroid-insensitive -- SLE systemic lupus erythematosus -- TRAF TNF receptor-associated factor -- TXNIP thioredoxin-interacting protein; Inflammasome -- Asthma -- Chronic obstructive pulmonary disease -- IL-1β -- Lung; Immunochemistry -- Periodicals; Molecular biology -- Periodicals; Immunochemistry -- Periodicals; Allergy and Immunology -- Periodicals; Molecular Biology -- Periodicals; Immunochimie -- Périodiques; Biologie moléculaire -- Périodiques; Immunochemistry; Molecular biology; Periodicals; Electronic journals; 571.96
• DOI: 10.1016/j.molimm.2017.01.014
• Languages: English
• ISSNs: 0161-5890

Abstract

Highlights: Activation of the inflammasome plays a critical role in the innate immune response against noxious stimuli in the lung. Excessive activation of the inflammasome may be associated with the development of chronic lung diseases. Inflammasome-targeted, site-specific therapeutics may be beneficial in suppressing inflammasome-associated disease. Abstract: Innate immune responses act as first line defences upon exposure to potentially noxious stimuli. The innate immune system has evolved numerous intracellular and extracellular receptors that undertake surveillance for potentially damaging particulates. Inflammasomes are intracellular innate immune multiprotein complexes that form and are activated following interaction with these stimuli. Inflammasome activation leads to the cleavage of pro-IL-1β and release of the pro-inflammatory cytokine, IL-1β, which initiates acute phase pro-inflammatory responses, and other responses are also involved (IL-18, pyroptosis). However, excessive activation of inflammasomes can result in chronic inflammation, which has been implicated in a range of chronic inflammatory diseases. The airways are constantly exposed to a wide variety of stimuli. Inflammasome activation and downstream responses clears these stimuli. However, excessive activation may drive the pathogenesis of chronic respiratory diseases such as severe asthma and chronic obstructive pulmonary disease. Thus, there is currently intense interest in the role of inflammasomes in chronic inflammatory lung diseases and in their potential for therapeutic targeting. Here we review the known associations between inflammasome-mediated responses and the development and exacerbation of chronic lung diseases.