scholarly journals House dust mite exposure attenuates influenza A infection in a mouse model of pulmonary allergic inflammation

2019 ◽  
Vol 129 ◽  
pp. 242-249
Author(s):  
Qiyao Hu ◽  
Ryan P. Gilley ◽  
Peter H. Dube
Keyword(s):  
Mouse Model ◽  
House Dust ◽  
House Dust Mite ◽  
Influenza A ◽  
Allergic Inflammation ◽  
Dust Mite ◽  
Pulmonary Allergic Inflammation

scholarly journals Berberine reduce allergic inflammation in a house dust mite allergic rhinitis mouse model

2015 ◽  
Vol 53 (4) ◽  
pp. 353-358 ◽  
Author(s):  
B.Y. KIm ◽  
H.R. Park ◽  
H.G. Jeong ◽  
S.W. Kim
Keyword(s):  
Allergic Rhinitis ◽  
Mouse Model ◽  
House Dust ◽  
House Dust Mite ◽  
Allergic Inflammation ◽  
Dust Mite

scholarly journals Airway epithelial cell necroptosis contributes to asthma exacerbation in a mouse model of house dust mite-induced allergic inflammation

2021 ◽  
Author(s):  
Nikos Oikonomou ◽  
Martjin J. Schuijs ◽  
Antonis Chatzigiagkos ◽  
Ariadne Androulidaki ◽  
Vassilis Aidinis ◽  
...  
Keyword(s):  
Cell Death ◽  
Epithelial Cell ◽  
Mouse Model ◽  
House Dust ◽  
House Dust Mite ◽  
Airway Epithelial Cell ◽  
Allergic Inflammation ◽  
Airway Epithelial ◽  
Dust Mite

AbstractRegulation 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 FADDAEC-KO mice, suggesting that necroptosis of FADD-deficient AECs augmented the allergic immune response. These results reveal a role of AEC necroptosis in amplifying airway allergic inflammation and suggest that necroptosis could contribute to asthma exacerbations caused by respiratory virus infections inducing AEC death.

Deficiency of CARS2, a principal cysteine persulfide synthase, aggravated house dust mite-induced allergic inflammation in a mouse model of asthma

2020 ◽  
Author(s):  
Yusaku Sasaki ◽  
Mituhiro Yamada ◽  
Tadahisa Numakura ◽  
Tomoaki Ida ◽  
Masanobu Morita ◽  
...  
Keyword(s):  
Mouse Model ◽  
House Dust ◽  
House Dust Mite ◽  
Allergic Inflammation ◽  
Dust Mite

scholarly journals House Dust Mite-Specific Sublingual Immunotherapy Prevents the Development of Allergic Inflammation in a Mouse Model of Experimental Asthma

2016 ◽  
Vol 170 (1) ◽  
pp. 22-34 ◽  
Author(s):  
Stefanie Hagner ◽  
Carola Rask ◽  
Jens Brimnes ◽  
Peter Sejer Andersen ◽  
Hartmann Raifer ◽  
...  
Keyword(s):  
Mouse Model ◽  
House Dust ◽  
House Dust Mite ◽  
Sublingual Immunotherapy ◽  
Allergic Inflammation ◽  
Dust Mite

scholarly journals G Protein-Coupled Receptor Kinase 2 (GRK2) Regulates T Cell Response in a Murine Model of House Dust Mite-Induced Asthma

2021 ◽  
Vol 2 ◽  
Author(s):  
Ananth K. Kammala ◽  
Canchai Yang ◽  
Reynold A. Panettieri ◽  
Rupali Das ◽  
Hariharan Subramanian
Keyword(s):  
T Cell ◽  
Mouse Model ◽  
G Protein ◽  
House Dust ◽  
House Dust Mite ◽  
T Cell Response ◽  
Receptor Kinase ◽  
G Protein Coupled Receptor ◽  
Dust Mite ◽  
G Protein Coupled

G protein-coupled receptor kinase 2 (GRK2) is an adapter protein that modulates G protein-coupled receptor (GPCR) signaling. It also regulates the functions and activity of other intracellular proteins in many cell types. Accordingly, GRK2 is thought to contribute to disease progression by a variety of mechanisms related to its multifunctional roles. Indeed, GRK2 levels are enhanced in patient samples as well as in preclinical models of several diseases. We have previously shown that GRK2 regulates mast cell functions, and thereby contributes to exacerbated inflammation during allergic reactions. In the current study, we observed that GRK2 levels are enhanced in the lungs of human asthma patients and in mice sensitized to house dust mite extract (HDME) allergen. Consistent with these findings, interleukin (IL)-4 and IL-13 levels were reduced in the lungs of GRK2+/− mice in a HMDE mouse model of asthma. Because Th2 cells are the major source of these cytokines during asthma, we determined the role of GRK2 in regulating T cell-specific responses in our HMDE mouse model. We observed a significant reduction of airway hyperresponsiveness (AHR), lung eosinophil and lymphocyte counts, serum IgE, Th2 cytokines (IL-4 and IL-13), goblet cell hyperplasia and mucus production in mice that had reduced GRK2 expression specifically in T cells. Collectively, our studies reveal an important role for GRK2 in regulating T cell response during asthma pathogenesis and further elucidation of the mechanisms through which GRK2 modulates airway inflammation will lead to the development of new therapeutic strategies for asthma.

scholarly journals Influenza A facilitates sensitization to house dust mite in infant mice leading to an asthma phenotype in adulthood

2011 ◽  
Vol 4 (6) ◽  
pp. 682-694 ◽  
Author(s):  
A Al-Garawi ◽  
R Fattouh ◽  
F Botelho ◽  
T D Walker ◽  
S Goncharova ◽  
...  
Keyword(s):  
House Dust ◽  
House Dust Mite ◽  
Influenza A ◽  
Asthma Phenotype ◽  
Dust Mite
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