The nucleotide-binding domain, leucine-rich repeat protein 3 inflammasome/IL-1 receptor I axis mediates innate, but not adaptive, immune responses after exposure to particulate matter under 10 μm.
Identifieur interne : 000496 ( Main/Curation ); précédent : 000495; suivant : 000497The nucleotide-binding domain, leucine-rich repeat protein 3 inflammasome/IL-1 receptor I axis mediates innate, but not adaptive, immune responses after exposure to particulate matter under 10 μm.
Auteurs : Jeremy A. Hirota ; Matthew J. Gold ; Paul R. Hiebert ; Leigh G. Parkinson ; Tracee Wee ; Dirk Smith ; Phil M. Hansbro ; Chris Carlsten ; Stephan Vaneeden ; Don D. Sin ; Kelly M. Mcnagny ; Darryl A. KnightSource :
- American journal of respiratory cell and molecular biology [ 1535-4989 ] ; 2015.
English descriptors
- KwdEn :
- Adaptive Immunity (drug effects), Animals, Asthma (chemically induced), Asthma (immunology), Asthma (pathology), Carrier Proteins (immunology), Cell Line, Transformed, Cytokines (immunology), Dendritic Cells (immunology), Dendritic Cells (pathology), Humans, Immunity, Innate (drug effects), Inflammasomes (immunology), Mice, Mice, Inbred BALB C, NLR Family, Pyrin Domain-Containing 3 Protein, Particulate Matter (adverse effects), Particulate Matter (pharmacology), Receptors, Interleukin-1 Type I (immunology), Respiratory Mucosa (immunology), Respiratory Mucosa (pathology), Signal Transduction (immunology).
- MESH :
- chemical , adverse effects : Particulate Matter.
- chemical , immunology : Carrier Proteins, Cytokines, Inflammasomes, Receptors, Interleukin-1 Type I.
- chemically induced : Asthma.
- drug effects : Adaptive Immunity, Immunity, Innate.
- immunology : Asthma, Dendritic Cells, Respiratory Mucosa, Signal Transduction.
- pathology : Asthma, Dendritic Cells, Respiratory Mucosa.
- chemical , pharmacology : Particulate Matter.
- Animals, Cell Line, Transformed, Humans, Mice, Mice, Inbred BALB C, NLR Family, Pyrin Domain-Containing 3 Protein.
Abstract
Exposure to particulate matter (PM), a major component of air pollution, contributes to increased morbidity and mortality worldwide. Inhaled PM induces innate immune responses by airway epithelial cells that may lead to the exacerbation or de novo development of airway disease. We have previously shown that 10-μm PM (PM10) activates the nucleotide-binding domain, leucine-rich repeat protein (NLRP) 3 inflammasome in human airway epithelial cells. Our objective was to determine the innate and adaptive immune responses mediated by the airway epithelium NLRP3 inflammasome in response to PM10 exposure. Using in vitro cultures of human airway epithelial cells and in vivo studies with wild-type and Nlrp3(-/-) mice, we investigated the downstream consequences of PM10-induced NLPR3 inflammasome activation on cytokine production, cellular inflammation, dendritic cell activation, and PM10-facilitated allergic sensitization. PM10 activates an NLRP3 inflammasome/IL-1 receptor I (IL-1RI) axis in airway epithelial cells, resulting in IL-1β, CC chemokine ligand-20, and granulocyte/macrophage colony-stimulating factor production, which is associated with dendritic cell activation and lung neutrophilia. Despite these profound innate immune responses in the airway epithelium, the NLRP3 inflammasome/IL-1RI axis is dispensable for PM10-facilitated allergic sensitization. We demonstrate the importance of the lung NLRP3 inflammasome in mediating PM10 exposure-associated innate, but not adaptive, immune responses. Our study highlights a mechanism by which PM10 exposure can contribute to the exacerbation of airway disease, but not PM10-facilitated allergic sensitization.
DOI: 10.1165/rcmb.2014-0158OC
PubMed: 24988285
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Jeremy A. Hirota<affiliation><nlm:affiliation>1 James Hogg Research Centre.</nlm:affiliation>
<wicri:noCountry code="no comma">1 James Hogg Research Centre.</wicri:noCountry>
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Le document en format XML
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<term>Asthma (chemically induced)</term>
<term>Asthma (immunology)</term>
<term>Asthma (pathology)</term>
<term>Carrier Proteins (immunology)</term>
<term>Cell Line, Transformed</term>
<term>Cytokines (immunology)</term>
<term>Dendritic Cells (immunology)</term>
<term>Dendritic Cells (pathology)</term>
<term>Humans</term>
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<term>Receptors, Interleukin-1 Type I (immunology)</term>
<term>Respiratory Mucosa (immunology)</term>
<term>Respiratory Mucosa (pathology)</term>
<term>Signal Transduction (immunology)</term>
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<term>Cytokines</term>
<term>Inflammasomes</term>
<term>Receptors, Interleukin-1 Type I</term>
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<term>Respiratory Mucosa</term>
<term>Signal Transduction</term>
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<term>Respiratory Mucosa</term>
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<front><div type="abstract" xml:lang="en">Exposure to particulate matter (PM), a major component of air pollution, contributes to increased morbidity and mortality worldwide. Inhaled PM induces innate immune responses by airway epithelial cells that may lead to the exacerbation or de novo development of airway disease. We have previously shown that 10-μm PM (PM10) activates the nucleotide-binding domain, leucine-rich repeat protein (NLRP) 3 inflammasome in human airway epithelial cells. Our objective was to determine the innate and adaptive immune responses mediated by the airway epithelium NLRP3 inflammasome in response to PM10 exposure. Using in vitro cultures of human airway epithelial cells and in vivo studies with wild-type and Nlrp3(-/-) mice, we investigated the downstream consequences of PM10-induced NLPR3 inflammasome activation on cytokine production, cellular inflammation, dendritic cell activation, and PM10-facilitated allergic sensitization. PM10 activates an NLRP3 inflammasome/IL-1 receptor I (IL-1RI) axis in airway epithelial cells, resulting in IL-1β, CC chemokine ligand-20, and granulocyte/macrophage colony-stimulating factor production, which is associated with dendritic cell activation and lung neutrophilia. Despite these profound innate immune responses in the airway epithelium, the NLRP3 inflammasome/IL-1RI axis is dispensable for PM10-facilitated allergic sensitization. We demonstrate the importance of the lung NLRP3 inflammasome in mediating PM10 exposure-associated innate, but not adaptive, immune responses. Our study highlights a mechanism by which PM10 exposure can contribute to the exacerbation of airway disease, but not PM10-facilitated allergic sensitization.</div>
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