scholarly journals The composition of house dust mite is critical for mucosal barrier dysfunction and allergic sensitisation

Thorax ◽  
2011 ◽  
Vol 67 (6) ◽  
pp. 488-495 ◽  
Author(s):  
S Post ◽  
M C Nawijn ◽  
T L Hackett ◽  
M Baranowska ◽  
R Gras ◽  
...  
Keyword(s):  
House Dust ◽  
House Dust Mite ◽  
Mucosal Barrier ◽  
Barrier Dysfunction ◽  
Allergic Sensitisation ◽  
Dust Mite

House dust mite-induced ATP release plays a role in the innate immunological response and barrier dysfunction of airway epithelium

Pneumologie ◽  
2012 ◽  
Vol 66 (11) ◽  
Author(s):  
S Post ◽  
M Nawijn ◽  
A van Oosterhout ◽  
I Heijink
Keyword(s):  
House Dust ◽  
House Dust Mite ◽  
Airway Epithelium ◽  
Atp Release ◽  
Immunological Response ◽  
Barrier Dysfunction ◽  
Dust Mite

House dust mite-induced calcium signaling instigates epithelial barrier dysfunction and CCL20 production

Allergy ◽  
2013 ◽  
pp. n/a-n/a ◽  
Author(s):  
S. Post ◽  
M. C. Nawijn ◽  
M. R. Jonker ◽  
N. Kliphuis ◽  
M. van den Berge ◽  
...  
Keyword(s):  
Calcium Signaling ◽  
House Dust ◽  
House Dust Mite ◽  
Epithelial Barrier ◽  
Barrier Dysfunction ◽  
Dust Mite ◽  
Epithelial Barrier Dysfunction

Stress, asthma and allergic sensitisation to house dust mite in children

2021 ◽  
Vol 25 (8) ◽  
pp. 675-676
Author(s):  
I. Annesi-Maesano ◽  
S. Banerjee ◽  
N. Pham-Thi ◽  
on behalf of the French 6 City Study Group
Keyword(s):  
House Dust ◽  
House Dust Mite ◽  
Allergic Sensitisation ◽  
Dust Mite

Airborne Formaldehyde Exacerbates Skin Barrier Dysfunction in NC/Nga Mice With House Dust Mite-induced Atopic Dermatitis

2018 ◽  
Vol 141 (2) ◽  
pp. AB133
Author(s):  
Kangmo Ahn ◽  
Ei-Seul Na ◽  
Jihyun Kim ◽  
Ji-Yun Kim
Keyword(s):  
Atopic Dermatitis ◽  
House Dust ◽  
House Dust Mite ◽  
Skin Barrier ◽  
Barrier Dysfunction ◽  
Dust Mite

1,25-Dihydroxyvitamin D3 targeting VEGF pathway alleviates house dust mite (HDM)-induced airway epithelial barrier dysfunction

2017 ◽  
Vol 312 ◽  
pp. 15-24 ◽  
Author(s):  
Ruhui Zhang ◽  
Hangming Dong ◽  
Haijin Zhao ◽  
Liqin Zhou ◽  
Fei Zou ◽  
...  
Keyword(s):  
House Dust ◽  
House Dust Mite ◽  
Epithelial Barrier ◽  
Airway Epithelial ◽  
Barrier Dysfunction ◽  
Dihydroxyvitamin D3 ◽  
1,25 Dihydroxyvitamin D3 ◽  
Dust Mite ◽  
Vegf Pathway ◽  
Epithelial Barrier Dysfunction

Nuclear erythroid 2-related factor 2 activation inhibits house dust mite-induced sinonasal epithelial cell barrier dysfunction

2017 ◽  
Vol 7 (5) ◽  
pp. 536-541 ◽  
Author(s):  
Nyall R. London ◽  
Anuj Tharakan ◽  
Andrew P. Lane ◽  
Shyam Biswal ◽  
Murugappan Ramanathan
Keyword(s):  
Epithelial Cell ◽  
House Dust ◽  
House Dust Mite ◽  
Related Factor ◽  
Barrier Dysfunction ◽  
Dust Mite

scholarly journals Correction to: PGC-1α regulates airway epithelial barrier dysfunction induced by house dust mite

2021 ◽  
Vol 22 (1) ◽  
Author(s):  
Tsutomu Saito ◽  
Tomohiro Ichikawa ◽  
Tadahisa Numakura ◽  
Mitsuhiro Yamada ◽  
Akira Koarai ◽  
...  
Keyword(s):  
House Dust ◽  
House Dust Mite ◽  
Epithelial Barrier ◽  
Airway Epithelial ◽  
Barrier Dysfunction ◽  
Dust Mite ◽  
Epithelial Barrier Dysfunction

An amendment to this paper has been published and can be accessed via the original article.

scholarly journals PGC-1α Regulates Airway Epithelial Barrier Dysfunction Induced by House Dust Mite.

2020 ◽  
Author(s):  
Tsutomu Saito ◽  
Tomohiro Ichikawa ◽  
Tadahisa Numakura ◽  
Mitsuhiro Yamada ◽  
Akira Koarai ◽  
...  
Keyword(s):  
Mitochondrial Biogenesis ◽  
House Dust ◽  
House Dust Mite ◽  
Barrier Function ◽  
Epithelial Barrier ◽  
Peroxisome Proliferator ◽  
Airway Epithelial ◽  
Barrier Dysfunction ◽  
Dust Mite ◽  
E Cadherin

Abstract Background: The airway epithelial barrier function is disrupted in the airways of asthmatic patients. Abnormal mitochondrial biogenesis is reportedly involved in the pathogenesis of asthma. However, the role of mitochondrial biogenesis in the airway barrier dysfunction has not been elucidated yet. This study aimed to clarify whether the peroxisome proliferator-activated receptor γ coactivator-1alpha (PGC-1α), a central regulator of mitochondrial biogenesis, is involved in the disruption of the airway barrier function induced by aeroallergens. Methods: BEAS-2B cells were exposed to house dust mite (HDM) and the expressions of PGC-1α and E-cadherin, a junctional protein, were examined by immunoblotting. The effect of SRT1720, a PGC-1α activator, was investigated by immunoblotting, immunocytochemistry, and measuring the transepithelial electrical resistance (TEER) on the HDM-induced reduction in mitochondrial biogenesis markers and junctional proteins in airway bronchial epithelial cells. Furthermore,the effects of protease activated receptor 2 (PAR2) inhibitor, GB83, Toll-like receptor 4 (TLR4) inhibitor, lipopolysaccharide from Rhodobacter sphaeroides (LPS-RS), protease inhibitors including E64 and 4-(2-Aminoethyl) benzenesulfonyl fluoride hydrochloride (AEBSF) on the HDM-induced barrier dysfunction were investigated. Results: The amounts of PGC-1α and E-cadherin in the HDM-treated cells were significantly decreased compared to the vehicle-treated cells. SRT1720 restored the expressions of PGC-1α and E-cadherin reduced by HDM in BEAS-2B cells. Treatment with SRT1720 also significantly ameliorated the HDM-induced reduction in TEER. In addition, GB83, LPS-RS, E64 and AEBSF prevented the HDM-induced reduction in the expression of PGC1α and E-cadherin. Conclusions: The current study demonstrated that HDM disrupted the airway barrier function through the PAR2/TLR4/PGC-1α-dependent pathway. The modulation of this pathway could be a new approach for the treatment of asthma.

scholarly journals PGC-1α regulates airway epithelial barrier dysfunction induced by house dust mite

2021 ◽  
Vol 22 (1) ◽  
Author(s):  
Tsutomu Saito ◽  
Tomohiro Ichikawa ◽  
Tadahisa Numakura ◽  
Mitsuhiro Yamada ◽  
Akira Koarai ◽  
...  
Keyword(s):  
Mitochondrial Biogenesis ◽  
House Dust ◽  
House Dust Mite ◽  
Barrier Function ◽  
Epithelial Barrier ◽  
Peroxisome Proliferator ◽  
Airway Epithelial ◽  
Barrier Dysfunction ◽  
Dust Mite ◽  
E Cadherin

Abstract Background The airway epithelial barrier function is disrupted in the airways of asthmatic patients. Abnormal mitochondrial biogenesis is reportedly involved in the pathogenesis of asthma. However, the role of mitochondrial biogenesis in the airway barrier dysfunction has not been elucidated yet. This study aimed to clarify whether the peroxisome proliferator-activated receptor γ coactivator-1alpha (PGC-1α), a central regulator of mitochondrial biogenesis, is involved in the disruption of the airway barrier function induced by aeroallergens. Methods BEAS-2B cells were exposed to house dust mite (HDM) and the expressions of PGC-1α and E-cadherin, a junctional protein, were examined by immunoblotting. The effect of SRT1720, a PGC-1α activator, was investigated by immunoblotting, immunocytochemistry, and measuring the transepithelial electrical resistance (TEER) on the HDM-induced reduction in mitochondrial biogenesis markers and junctional proteins in airway bronchial epithelial cells. Furthermore,the effects of protease activated receptor 2 (PAR2) inhibitor, GB83, Toll-like receptor 4 (TLR4) inhibitor, lipopolysaccharide from Rhodobacter sphaeroides (LPS-RS), protease inhibitors including E64 and 4-(2-Aminoethyl) benzenesulfonyl fluoride hydrochloride (AEBSF) on the HDM-induced barrier dysfunction were investigated. Results The amounts of PGC-1α and E-cadherin in the HDM-treated cells were significantly decreased compared to the vehicle-treated cells. SRT1720 restored the expressions of PGC-1α and E-cadherin reduced by HDM in BEAS-2B cells. Treatment with SRT1720 also significantly ameliorated the HDM-induced reduction in TEER. In addition, GB83, LPS-RS, E64 and AEBSF prevented the HDM-induced reduction in the expression of PGC1α and E-cadherin. Conclusions The current study demonstrated that HDM disrupted the airway barrier function through the PAR2/TLR4/PGC-1α-dependent pathway. The modulation of this pathway could be a new approach for the treatment of asthma.

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