Airway epithelial cell necroptosis contributes to asthma exacerbation in a mouse model of house dust mite-induced allergic inflammation.
Airway Remodeling
Allergens
/ immunology
Animals
Asthma
/ etiology
Basic Helix-Loop-Helix Transcription Factors
/ metabolism
Biomarkers
Disease Models, Animal
Disease Progression
Disease Susceptibility
Enzyme Activation
Fas-Associated Death Domain Protein
/ deficiency
Immunoglobulin E
/ immunology
Immunohistochemistry
Mice
Mice, Knockout
Necroptosis
/ immunology
Pyroglyphidae
/ immunology
Receptor-Interacting Protein Serine-Threonine Kinases
/ metabolism
Receptors, Aryl Hydrocarbon
/ metabolism
Respiratory Mucosa
/ immunology
Journal
Mucosal immunology
ISSN: 1935-3456
Titre abrégé: Mucosal Immunol
Pays: United States
ID NLM: 101299742
Informations de publication
Date de publication:
09 2021
09 2021
Historique:
received:
30
11
2020
accepted:
06
05
2021
revised:
02
05
2021
pubmed:
29
5
2021
medline:
22
1
2022
entrez:
28
5
2021
Statut:
ppublish
Résumé
Regulation of epithelial cell death has emerged as a key mechanism controlling immune homeostasis in barrier surfaces. Necroptosis is a type of regulated necrotic cell death induced by receptor interacting protein kinase 3 (RIPK3) that has been shown to cause inflammatory pathologies in different tissues. The role of regulated cell death and particularly necroptosis in lung homeostasis and disease remains poorly understood. Here we show that mice with Airway Epithelial Cell (AEC)-specific deficiency of Fas-associated with death domain (FADD), an adapter essential for caspase-8 activation, developed exacerbated allergic airway inflammation in a mouse model of asthma induced by sensitization and challenge with house dust mite (HDM) extracts. Genetic inhibition of RIPK1 kinase activity by crossing to mice expressing kinase inactive RIPK1 as well as RIPK3 or MLKL deficiency prevented the development of exaggerated HDM-induced asthma pathology in FADD
Identifiants
pubmed: 34045680
doi: 10.1038/s41385-021-00415-5
pii: S1933-0219(22)00210-0
pmc: PMC8379077
doi:
Substances chimiques
Ahr protein, mouse
0
Allergens
0
Basic Helix-Loop-Helix Transcription Factors
0
Biomarkers
0
Fadd protein, mouse
0
Fas-Associated Death Domain Protein
0
Receptors, Aryl Hydrocarbon
0
Immunoglobulin E
37341-29-0
Receptor-Interacting Protein Serine-Threonine Kinases
EC 2.7.11.1
Ripk1 protein, mouse
EC 2.7.11.1
Ripk3 protein, mouse
EC 2.7.11.1
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
1160-1171Commentaires et corrections
Type : CommentIn
Informations de copyright
© 2021. The Author(s).
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