Literature DB >> 28129896

Inflammasomes in the lung.

James W Pinkerton1, Richard Y Kim1, Avril A B Robertson2, Jeremy A Hirota3, Lisa G Wood1, Darryl A Knight1, Matthew A Cooper2, Luke A J O'Neill4, Jay C Horvat1, Philip M Hansbro5.   

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.
Copyright © 2017 Elsevier Ltd. All rights reserved.

Entities:  

Keywords:  Asthma; Chronic obstructive pulmonary disease; IL-1β; Inflammasome; Lung

Mesh:

Substances:

Year:  2017        PMID: 28129896     DOI: 10.1016/j.molimm.2017.01.014

Source DB:  PubMed          Journal:  Mol Immunol        ISSN: 0161-5890            Impact factor:   4.407


  47 in total

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4.  The role of IL-1 family of cytokines and receptors in pathogenesis of COVID-19.

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Authors:  Davinder Kaur; Latifa Chachi; Edith Gomez; Nicolas Sylvius; Christopher E Brightling
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8.  Apolipoprotein E is a concentration-dependent pulmonary danger signal that activates the NLRP3 inflammasome and IL-1β secretion by bronchoalveolar fluid macrophages from asthmatic subjects.

Authors:  Elizabeth M Gordon; Xianglan Yao; Haitao Xu; William Karkowsky; Maryann Kaler; Or Kalchiem-Dekel; Amisha V Barochia; Meixia Gao; Karen J Keeran; Kenneth R Jeffries; Stewart J Levine
Journal:  J Allergy Clin Immunol       Date:  2019-03-11       Impact factor: 14.290

9.  Mechanisms of Environment-Induced Autoimmunity.

Authors:  K Michael Pollard; David M Cauvi; Jessica M Mayeux; Christopher B Toomey; Amy K Peiss; Per Hultman; Dwight H Kono
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10.  Schisandrin B Attenuates Airway Inflammation and Airway Remodeling in Asthma by Inhibiting NLRP3 Inflammasome Activation and Reducing Pyroptosis.

Authors:  Xiufeng Chen; Zhen Xiao; Zhiyan Jiang; Yonghong Jiang; Wen Li; Mingjing Wang
Journal:  Inflammation       Date:  2021-06-18       Impact factor: 4.092

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