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Am J Pathol. 2014 Jan;184(1):42-54. doi: 10.1016/j.ajpath.2013.09.007. Epub 2013 Oct 30.

New insights into mechanisms controlling the NLRP3 inflammasome and its role in lung disease.

Author information

1
Institute of Innate Immunity, University Hospital, University of Bonn, Bonn, Germany.
2
Institute of Innate Immunity, University Hospital, University of Bonn, Bonn, Germany; German Center for Neurodegenerative Diseases (DZNE), Bonn, Germany; Division of Infectious Diseases and Immunology, Department of Medicine, University of Massachusetts Medical School, Worcester, Massachusetts. Electronic address: eicke.latz@uni-bonn.de.

Abstract

Inflammasomes are large macromolecular signaling complexes that control the proteolytic activation of two highly proinflammatory IL-1 family cytokines, IL-1β and IL-18. The NLRP3 inflammasome is of special interest because it can assemble in response to a diverse array of stimuli and because the inflammation it triggers has been implicated in a wide variety of disease pathologies. To avoid aberrant activation, the NLRP3 inflammasome is modulated on multiple levels, ranging from transcriptional control to post-translational protein modifications. Emerging genetic and pharmacological evidence suggests that NLRP3 inflammasome activation may also be involved in acute lung inflammation after viral infection and during progression of several chronic pulmonary diseases, including idiopathic pulmonary fibrosis, chronic obstructive pulmonary disease, and asthma. Here, we review the most recent contributions to our understanding of the regulatory mechanisms controlling activation of the NLRP3 inflammasome and discuss the contribution of the NLRP3 inflammasome to the pathology of lung diseases.

PMID:
24183846
PMCID:
PMC3873477
DOI:
10.1016/j.ajpath.2013.09.007
[Indexed for MEDLINE]
Free PMC Article

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