NDLI: Critical role for the NLRP3 inflammasome during acute lung $injury^{}$

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Critical role for the NLRP3 inflammasome during acute lung $injury^{}$

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Dhond, Rasika M. Andjelkovic, Anuska V. Canning, Bethany A. Grailer, Jamison J. Zetoune, Firas S. Ward, Peter A. Kalbitz, Miriam Haggadone, Mikel D.
Description	Author Affiliation: Grailer JJ ( Department of Pathology, University of Michigan Medical School, Ann Arbor, MI 48109.); Canning BA ( Department of Pathology, University of Michigan Medical School, Ann Arbor, MI 48109.); Kalbitz M ( Department of Pathology, University of Michigan Medical School, Ann Arbor, MI 48109.); Haggadone MD ( Department of Pathology, University of Michigan Medical School, Ann Arbor, MI 48109.); Dhond RM ( Department of Pathology, University of Michigan Medical School, Ann Arbor, MI 48109.); Andjelkovic AV ( Department of Pathology, University of Michigan Medical School, Ann Arbor, MI 48109.); Zetoune FS ( Department of Pathology, University of Michigan Medical School, Ann Arbor, MI 48109.); Ward PA ( Department of Pathology, University of Michigan Medical School, Ann Arbor, MI 48109 pward@med.umich.edu.)
Abstract	The inflammasome is a key factor in innate immunity and senses soluble pathogen and danger-associated molecular patterns as well as biological crystals (urate, cholesterol, etc.), resulting in expression of IL-1ß and IL-18. Using a standard model of acute lung injury (ALI) in mice featuring airway instillation of LPS, ALI was dependent on availability of NLRP3 as well as caspase-1, which are known features of the NLRP3 inflammasome. The appearance of IL-1ß, a product of NLRP3 inflammasome activation, was detected in bronchoalveolar lavage fluids (BALF) in a macrophage- and neutrophil-dependent manner. Neutrophil-derived extracellular histones appeared in the BALF during ALI and directly activated the NLRP3 inflammasome. Ab-mediated neutralization of histones significantly reduced IL-1ß levels in BALF during ALI. Inflammasome activation by extracellular histones in LPS-primed macrophages required NLRP3 and caspase-1 as well as extrusion of K(+), increased intracellular Ca(2+) concentration, and generation of reactive oxygen species. NLRP3 and caspase-1 were also required for full extracellular histone presence during ALI, suggesting a positive feedback mechanism. Extracellular histone and IL-1ß levels in BALF were also elevated in C5a-induced and IgG immune complex ALI models, suggesting a common inflammatory mechanism. These data indicate an interaction between extracellular histones and the NLRP3 inflammasome, resulting in ALI. Such findings suggest novel targets for treatment of ALI, for which there is currently no known efficacious drug.
ISSN	00221767
e-ISSN	15506606
DOI	10.4049/jimmunol.1400368
Journal	The Journal of Immunology
Issue Number	12
Volume Number	192
Language	English
Publisher	The American Association of Immunologists
Publisher Date	2014-06-15
Publisher Place	United States
Access Restriction	Open
Subject Keyword	Acute Lung Injury Immunology Carrier Proteins Inflammasomes Macrophages, Alveolar Neutrophils Chemically Induced Genetics Pathology Animals Bronchoalveolar Lavage Fluid Caspase 1 Disease Models, Animal Histones Interleukin-18 Interleukin-1beta Lipopolysaccharides Pharmacology Mice Mice, Knockout Research Support, N.i.h., Extramural Discipline Immunology
Content Type	Text
Resource Type	Article
Subject	Immunology and Allergy Immunology

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