Serum Amyloid A Activates the NLRP3 Inflammasome and Promotes Th17 Allergic Asthma in Mice

IL-1β is a cytokine critical to several inflammatory diseases in which pathogenic Th17 responses are implicated. Activation of the NLRP3 inflammasome by microbial and environmental stimuli can enable the caspase-1–dependent processing and secretion of IL-1β. The acute-phase protein serum amyloid A (...

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Published inThe Journal of immunology (1950) Vol. 187; no. 1; pp. 64 - 73
Main Authors Ather, Jennifer L, Ckless, Karina, Martin, Rebecca, Foley, Kathryn L, Suratt, Benjamin T, Boyson, Jonathan E, Fitzgerald, Katherine A, Flavell, Richard A, Eisenbarth, Stephanie C, Poynter, Matthew E
Format Journal Article
LanguageEnglish
Published England 01.07.2011
Subjects
Online AccessGet full text
ISSN0022-1767
1550-6606
1550-6606
DOI10.4049/jimmunol.1100500

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Abstract IL-1β is a cytokine critical to several inflammatory diseases in which pathogenic Th17 responses are implicated. Activation of the NLRP3 inflammasome by microbial and environmental stimuli can enable the caspase-1–dependent processing and secretion of IL-1β. The acute-phase protein serum amyloid A (SAA) is highly induced during inflammatory responses, wherein it participates in systemic modulation of innate and adaptive immune responses. Elevated levels of IL-1β, SAA, and IL-17 are present in subjects with severe allergic asthma, yet the mechanistic relationship among these mediators has yet to be identified. In this study, we demonstrate that Saa3 is expressed in the lungs of mice exposed to several mixed Th2/Th17-polarizing allergic sensitization regimens. SAA instillation into the lungs elicits robust TLR2-, MyD88-, and IL-1–dependent pulmonary neutrophilic inflammation. Furthermore, SAA drives production of IL-1α, IL-1β, IL-6, IL-23, and PGE2, causes dendritic cell (DC) maturation, and requires TLR2, MyD88, and the NLRP3 inflammasome for secretion of IL-1β by DCs and macrophages. CD4+ T cells polyclonally stimulated in the presence of conditioned media from SAA-exposed DCs produced IL-17, and the capacity of polyclonally stimulated splenocytes to secrete IL-17 is dependent upon IL-1, TLR2, and the NLRP3 inflammasome. Additionally, in a model of allergic airway inflammation, administration of SAA to the lungs functions as an adjuvant to sensitize mice to inhaled OVA, resulting in leukocyte influx after Ag challenge and a predominance of IL-17 production from restimulated splenocytes that is dependent upon IL-1R signaling.
AbstractList IL-1β is a cytokine critical to several inflammatory diseases in which pathogenic Th17 responses are implicated. Activation of the NLRP3 inflammasome by microbial and environmental stimuli can enable the caspase-1–dependent processing and secretion of IL-1β. The acute-phase protein serum amyloid A (SAA) is highly induced during inflammatory responses, wherein it participates in systemic modulation of innate and adaptive immune responses. Elevated levels of IL-1β, SAA, and IL-17 are present in subjects with severe allergic asthma, yet the mechanistic relationship among these mediators has yet to be identified. In this study, we demonstrate that Saa3 is expressed in the lungs of mice exposed to several mixed Th2/Th17-polarizing allergic sensitization regimens. SAA instillation into the lungs elicits robust TLR2-, MyD88-, and IL-1–dependent pulmonary neutrophilic inflammation. Furthermore, SAA drives production of IL-1α, IL-1β, IL-6, IL-23, and PGE2, causes dendritic cell (DC) maturation, and requires TLR2, MyD88, and the NLRP3 inflammasome for secretion of IL-1β by DCs and macrophages. CD4+ T cells polyclonally stimulated in the presence of conditioned media from SAA-exposed DCs produced IL-17, and the capacity of polyclonally stimulated splenocytes to secrete IL-17 is dependent upon IL-1, TLR2, and the NLRP3 inflammasome. Additionally, in a model of allergic airway inflammation, administration of SAA to the lungs functions as an adjuvant to sensitize mice to inhaled OVA, resulting in leukocyte influx after Ag challenge and a predominance of IL-17 production from restimulated splenocytes that is dependent upon IL-1R signaling.
IL-1β is a cytokine critical to several inflammatory diseases in which pathogenic Th17 responses are implicated. Activation of the NLRP3 inflammasome by microbial and environmental stimuli can enable the caspase-1-dependent processing and secretion of IL-1β. The acute-phase protein serum amyloid A (SAA) is highly induced during inflammatory responses, wherein it participates in systemic modulation of innate and adaptive immune responses. Elevated levels of IL-1β, SAA, and IL-17 are present in subjects with severe allergic asthma, yet the mechanistic relationship among these mediators has yet to be identified. In this study, we demonstrate that Saa3 is expressed in the lungs of mice exposed to several mixed Th2/Th17-polarizing allergic sensitization regimens. SAA instillation into the lungs elicits robust TLR2-, MyD88-, and IL-1-dependent pulmonary neutrophilic inflammation. Furthermore, SAA drives production of IL-1α, IL-1β, IL-6, IL-23, and PGE(2), causes dendritic cell (DC) maturation, and requires TLR2, MyD88, and the NLRP3 inflammasome for secretion of IL-1β by DCs and macrophages. CD4(+) T cells polyclonally stimulated in the presence of conditioned media from SAA-exposed DCs produced IL-17, and the capacity of polyclonally stimulated splenocytes to secrete IL-17 is dependent upon IL-1, TLR2, and the NLRP3 inflammasome. Additionally, in a model of allergic airway inflammation, administration of SAA to the lungs functions as an adjuvant to sensitize mice to inhaled OVA, resulting in leukocyte influx after Ag challenge and a predominance of IL-17 production from restimulated splenocytes that is dependent upon IL-1R signaling.IL-1β is a cytokine critical to several inflammatory diseases in which pathogenic Th17 responses are implicated. Activation of the NLRP3 inflammasome by microbial and environmental stimuli can enable the caspase-1-dependent processing and secretion of IL-1β. The acute-phase protein serum amyloid A (SAA) is highly induced during inflammatory responses, wherein it participates in systemic modulation of innate and adaptive immune responses. Elevated levels of IL-1β, SAA, and IL-17 are present in subjects with severe allergic asthma, yet the mechanistic relationship among these mediators has yet to be identified. In this study, we demonstrate that Saa3 is expressed in the lungs of mice exposed to several mixed Th2/Th17-polarizing allergic sensitization regimens. SAA instillation into the lungs elicits robust TLR2-, MyD88-, and IL-1-dependent pulmonary neutrophilic inflammation. Furthermore, SAA drives production of IL-1α, IL-1β, IL-6, IL-23, and PGE(2), causes dendritic cell (DC) maturation, and requires TLR2, MyD88, and the NLRP3 inflammasome for secretion of IL-1β by DCs and macrophages. CD4(+) T cells polyclonally stimulated in the presence of conditioned media from SAA-exposed DCs produced IL-17, and the capacity of polyclonally stimulated splenocytes to secrete IL-17 is dependent upon IL-1, TLR2, and the NLRP3 inflammasome. Additionally, in a model of allergic airway inflammation, administration of SAA to the lungs functions as an adjuvant to sensitize mice to inhaled OVA, resulting in leukocyte influx after Ag challenge and a predominance of IL-17 production from restimulated splenocytes that is dependent upon IL-1R signaling.
IL-1β is a cytokine critical to several inflammatory diseases in which pathogenic Th17 responses are implicated. Activation of the NLRP3 inflammasome by microbial and environmental stimuli can enable the caspase-1-dependent processing and secretion of IL-1β. The acute-phase protein serum amyloid A (SAA) is highly induced during inflammatory responses, wherein it participates in systemic modulation of innate and adaptive immune responses. Elevated levels of IL-1β, SAA, and IL-17 are present in subjects with severe allergic asthma, yet the mechanistic relationship among these mediators has yet to be identified. In this study, we demonstrate that Saa3 is expressed in the lungs of mice exposed to several mixed Th2/Th17-polarizing allergic sensitization regimens. SAA instillation into the lungs elicits robust TLR2-, MyD88-, and IL-1-dependent pulmonary neutrophilic inflammation. Furthermore, SAA drives production of IL-1α, IL-1β, IL-6, IL-23, and PGE(2), causes dendritic cell (DC) maturation, and requires TLR2, MyD88, and the NLRP3 inflammasome for secretion of IL-1β by DCs and macrophages. CD4(+) T cells polyclonally stimulated in the presence of conditioned media from SAA-exposed DCs produced IL-17, and the capacity of polyclonally stimulated splenocytes to secrete IL-17 is dependent upon IL-1, TLR2, and the NLRP3 inflammasome. Additionally, in a model of allergic airway inflammation, administration of SAA to the lungs functions as an adjuvant to sensitize mice to inhaled OVA, resulting in leukocyte influx after Ag challenge and a predominance of IL-17 production from restimulated splenocytes that is dependent upon IL-1R signaling.
IL-1 beta is a cytokine critical to several inflammatory diseases in which pathogenic Th17 responses are implicated. Activation of the NLRP3 inflammasome by microbial and environmental stimuli can enable the caspase-1-dependent processing and secretion of IL-1 beta . The acute-phase protein serum amyloid A (SAA) is highly induced during inflammatory responses, wherein it participates in systemic modulation of innate and adaptive immune responses. Elevated levels of IL-1 beta , SAA, and IL-17 are present in subjects with severe allergic asthma, yet the mechanistic relationship among these mediators has yet to be identified. In this study, we demonstrate that Saa3 is expressed in the lungs of mice exposed to several mixed Th2/Th17-polarizing allergic sensitization regimens. SAA instillation into the lungs elicits robust TLR2-, MyD88-, and IL-1-dependent pulmonary neutrophilic inflammation. Furthermore, SAA drives production of IL-1 alpha , IL-1 beta , IL-6, IL-23, and PGE2, causes dendritic cell (DC) maturation, and requires TLR2, MyD88, and the NLRP3 inflammasome for secretion of IL-1 beta by DCs and macrophages. CD4+ T cells polyclonally stimulated in the presence of conditioned media from SAA-exposed DCs produced IL-17, and the capacity of polyclonally stimulated splenocytes to secrete IL-17 is dependent upon IL-1, TLR2, and the NLRP3 inflammasome. Additionally, in a model of allergic airway inflammation, administration of SAA to the lungs functions as an adjuvant to sensitize mice to inhaled OVA, resulting in leukocyte influx after Ag challenge and a predominance of IL-17 production from restimulated splenocytes that is dependent upon IL-1R signaling.
Interleukin (IL)-1β is a cytokine critical to several inflammatory diseases in which pathogenic T H 17 responses are implicated. Activation of the NLRP3 inflammasome by microbial and environmental stimuli can enable the caspase-1 dependent processing and secretion of IL-1β. The acute phase protein serum amyloid A (SAA) is highly induced during inflammatory responses, wherein it participates in systemic modulation of innate and adaptive immune responses. Elevated levels of IL-1β, SAA, and IL-17 are present in subjects with severe allergic asthma, yet the mechanistic relationship between these mediators has yet to be identified. Herein, we demonstrate that Saa3 is expressed in the lung of mice exposed to several mixed Th2/Th17-polarizing allergic sensitization regimens. SAA instillation into the lungs elicits robust TLR2-, MyD88-, and IL-1-dependent pulmonary neutrophilic inflammation. Furthermore, SAA drives production of IL-1α, IL-1β, IL-6, IL-23, and PGE 2 , causes dendritic cell maturation, and requires TLR2, MyD88, and the NLRP3 inflammasome for secretion of IL-1β by dendritic cells and macrophages. CD4 + T cells polyclonally stimulated in the presence of conditioned media from SAA-exposed dendritic cells produced IL-17 and the capacity of polyclonally-stimulated splenocytes to secrete IL-17 is dependent upon IL-1, TLR2, and the NLRP3 inflammasome. Additionally, in a model of allergic airway inflammation, administration of SAA to the lungs functions as an adjuvant to sensitize mice to inhaled ovalbumin, resulting in leukocyte influx after antigen challenge and a predominance of IL-17 production from restimulated splenocytes that is dependent upon IL-1 receptor signaling.
Author Boyson, Jonathan E
Eisenbarth, Stephanie C
Flavell, Richard A
Suratt, Benjamin T
Foley, Kathryn L
Poynter, Matthew E
Martin, Rebecca
Fitzgerald, Katherine A
Ather, Jennifer L
Ckless, Karina
AuthorAffiliation Department of Laboratory Medicine, Yale University School of Medicine, New Haven, CT, USA, 06520
Department of Chemistry, SUNY Plattsburgh, Plattsburgh, NY, USA, 12901
Howard Hughes Medical Institute, Department of Immunobiology, Yale University School of Medicine, New Haven, CT, USA, 06520
Division of Infectious Diseases and Immunology, Department of Medicine, University of Massachusetts Medical School, Worchester, MA, USA, 01655
Department of Surgery, University of Vermont, Burlington, VT, USA 05405
Vermont Lung Center, Division of Pulmonary Disease and Critical Care, Department of Medicine, University of Vermont, Burlington, VT, USA 05405
AuthorAffiliation_xml – name: Department of Chemistry, SUNY Plattsburgh, Plattsburgh, NY, USA, 12901
– name: Department of Surgery, University of Vermont, Burlington, VT, USA 05405
– name: Vermont Lung Center, Division of Pulmonary Disease and Critical Care, Department of Medicine, University of Vermont, Burlington, VT, USA 05405
– name: Division of Infectious Diseases and Immunology, Department of Medicine, University of Massachusetts Medical School, Worchester, MA, USA, 01655
– name: Howard Hughes Medical Institute, Department of Immunobiology, Yale University School of Medicine, New Haven, CT, USA, 06520
– name: Department of Laboratory Medicine, Yale University School of Medicine, New Haven, CT, USA, 06520
Author_xml – sequence: 1
  givenname: Jennifer L
  surname: Ather
  fullname: Ather, Jennifer L
– sequence: 2
  givenname: Karina
  surname: Ckless
  fullname: Ckless, Karina
– sequence: 3
  givenname: Rebecca
  surname: Martin
  fullname: Martin, Rebecca
– sequence: 4
  givenname: Kathryn L
  surname: Foley
  fullname: Foley, Kathryn L
– sequence: 5
  givenname: Benjamin T
  surname: Suratt
  fullname: Suratt, Benjamin T
– sequence: 6
  givenname: Jonathan E
  surname: Boyson
  fullname: Boyson, Jonathan E
– sequence: 7
  givenname: Katherine A
  surname: Fitzgerald
  fullname: Fitzgerald, Katherine A
– sequence: 8
  givenname: Richard A
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  surname: Poynter
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BackLink https://www.ncbi.nlm.nih.gov/pubmed/21622869$$D View this record in MEDLINE/PubMed
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Snippet IL-1β is a cytokine critical to several inflammatory diseases in which pathogenic Th17 responses are implicated. Activation of the NLRP3 inflammasome by...
IL-1 beta is a cytokine critical to several inflammatory diseases in which pathogenic Th17 responses are implicated. Activation of the NLRP3 inflammasome by...
Interleukin (IL)-1β is a cytokine critical to several inflammatory diseases in which pathogenic T H 17 responses are implicated. Activation of the NLRP3...
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StartPage 64
SubjectTerms Allergens - genetics
Allergens - physiology
Animals
Carrier Proteins - genetics
Carrier Proteins - metabolism
Cell Polarity - genetics
Cell Polarity - immunology
Cells, Cultured
Dendritic Cells - immunology
Dendritic Cells - metabolism
Dendritic Cells - pathology
Disease Models, Animal
Epitopes, T-Lymphocyte - genetics
Epitopes, T-Lymphocyte - immunology
Inflammasomes - deficiency
Inflammasomes - genetics
Inflammasomes - metabolism
Interleukin 1 Receptor Antagonist Protein - administration & dosage
Interleukin-1alpha - antagonists & inhibitors
Interleukin-1alpha - physiology
Interleukin-1beta - metabolism
Interleukin-1beta - physiology
Mice
Mice, Inbred C57BL
Mice, Knockout
Mice, Transgenic
NLR Family, Pyrin Domain-Containing 3 Protein
Respiratory Hypersensitivity - immunology
Respiratory Hypersensitivity - metabolism
Respiratory Hypersensitivity - pathology
Respiratory Mucosa - immunology
Respiratory Mucosa - metabolism
Respiratory Mucosa - pathology
Serum Amyloid A Protein - physiology
Signal Transduction - genetics
Signal Transduction - immunology
Spleen - immunology
Spleen - metabolism
Spleen - pathology
Th17 Cells - immunology
Th17 Cells - metabolism
Th17 Cells - pathology
Toll-Like Receptor 2 - deficiency
Toll-Like Receptor 2 - genetics
Toll-Like Receptor 2 - physiology
Title Serum Amyloid A Activates the NLRP3 Inflammasome and Promotes Th17 Allergic Asthma in Mice
URI https://www.ncbi.nlm.nih.gov/pubmed/21622869
https://www.proquest.com/docview/873314680
https://www.proquest.com/docview/904471546
https://pubmed.ncbi.nlm.nih.gov/PMC3119761
Volume 187
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