scholarly journals IL-25 Could Be Involved in the Development of Allergic Rhinitis Sensitized to House Dust Mite

2017 ◽  
Vol 2017 ◽  
pp. 1-8 ◽  
Author(s):  
Dae Woo Kim ◽  
Dong-Kyu Kim ◽  
Kyoung Mi Eun ◽  
Jun-Sang Bae ◽  
Young-Jun Chung ◽  
...  
Keyword(s):  
Allergic Rhinitis ◽  
House Dust ◽  
House Dust Mite ◽  
Allergic Inflammation ◽  
In Vitro Study ◽  
High Dose ◽  
Human Nasal Epithelial Cells ◽  
Dust Mite

Background and Purpose. When house dust mite (HDM), a common allergen, comes into the mucosal membrane, it may stimulate innate immunity. However, the precise role of interleukin- (IL-) 25 in the development of HDM-induced nasal allergic inflammation is still unclear. Therefore, we investigated the role of IL-25 in allergic rhinitis (AR) patients sensitized to HDM. Methods. To confirm the production of IL-25 in human nasal epithelial cells (HNECs), we stimulated HNECs. IL-25 expression in the nasal mucosa from control, non-AR (NAR) patients, and HDM-sensitized AR patients was assessed using immunohistochemistry, and quantitative reverse transcription PCR. Correlations between IL-25 and other inflammatory markers were explored. Results. An in vitro study showed significantly elevated concentrations of IL-25 in the HNEC samples with highest doses of HDM. Nasal tissues from AR patients sensitized to HDM showed significantly higher IL-25 expression, compared to those from the control or NAR patients. Moreover, the expression of IL-25 in nasal tissues from AR patients sensitized to HDM was positively associated with Th2 markers, such as ECP and GATA3. Conclusions. IL-25 expression increased with high-dose HDM stimulation and was related to Th2 markers. Therefore, IL-25 neutralization might offer a new strategy for treating patients with HDM-sensitized AR.

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 In Vivo and In Vitro Studies of Th17 Response to Specific Immunotherapy in House Dust Mite-Induced Allergic Rhinitis Patients

PLoS ONE ◽  
2014 ◽  
Vol 9 (3) ◽  
pp. e91950 ◽  
Author(s):  
Chun Wei Li ◽  
Han Gui Lu ◽  
De Hua Chen ◽  
Zhi Bin Lin ◽  
De Yun Wang ◽  
...  
Keyword(s):  
Allergic Rhinitis ◽  
House Dust ◽  
House Dust Mite ◽  
Specific Immunotherapy ◽  
In Vitro Studies ◽  
Th17 Response ◽  
Dust Mite

scholarly journals GITRL on dendritic cells aggravates house dust mite-induced airway inflammation and airway hyperresponsiveness by modulating CD4+ T cell differentiation

2021 ◽  
Vol 22 (1) ◽  
Author(s):  
Yaping Wang ◽  
Kou Liao ◽  
Bo Liu ◽  
Chao Niu ◽  
Wenjing Zou ◽  
...  
Keyword(s):  
Dendritic Cells ◽  
Cell Differentiation ◽  
House Dust ◽  
House Dust Mite ◽  
Airway Hyperresponsiveness ◽  
T Cell Differentiation ◽  
Asthmatic Children ◽  
Dust Mite

Abstract Background Glucocorticoid-induced tumor necrosis factor receptor family-related protein ligand (GITRL) plays an important role in tumors, autoimmunity and inflammation. However, GITRL is not known to modulate the pathogenesis of allergic asthma. In this study, we investigated whether regulating GITRL expressed on dendritic cells (DCs) can prevent asthma and to elucidate its mechanism of action. Methods In vivo, the role of GITRL in modulating house dust mite (HDM)-induced asthma was assessed in adeno-associated virus (AAV)-shGITRL mice. In vitro, the role of GITRL expression by DCs was evaluated in LV-shGITRL bone marrow dendritic cells (BMDCs) under HDM stimulation. And the direct effect of GITRL was observed by stimulating splenocytes with GITRL protein. The effect of regulating GITRL on CD4+ T cell differentiation was detected. Further, GITRL mRNA in the peripheral blood of asthmatic children was tested. Results GITRL was significantly increased in HDM-challenged mice. In GITRL knockdown mice, allergen-induced airway inflammation, serum total IgE levels and airway hyperresponsiveness (AHR) were reduced. In vitro, GITRL expression on BMDCs was increased after HDM stimulation. Further, knocking down GITRL on DCs partially restored the balance of Th1/Th2 and Th17/Treg cells. Moreover, GITRL stimulation in vitro inhibited Treg cell differentiation and promoted Th2 and Th17 cell differentiation. Similarly, GITRL mRNA expression was increased in the peripheral blood from asthmatic children. Conclusions This study identified a novel role for GITRL expressed by DCs as a positive regulator of CD4+ T cells responses in asthma, which implicates that GITRL inhibitors may be a potential immunotherapy for asthma.

Cross-reactivity between terrestrial snails (Helix species) and house-dust mite (Dermatophagoides pteronyssinus). II. In vitro study

Allergy ◽  
1998 ◽  
Vol 53 (2) ◽  
pp. 151-158 ◽  
Author(s):  
L. Guilloux ◽  
D.-A. Vuitton ◽  
M. Delbourg ◽  
A. Lagier ◽  
B. Adessi ◽  
...  
Keyword(s):  
House Dust ◽  
House Dust Mite ◽  
In Vitro Study ◽  
Dermatophagoides Pteronyssinus ◽  
Cross Reactivity ◽  
Vitro Study ◽  
Dust Mite ◽  
Terrestrial Snails

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.

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