ADAM10 mediates the house dust mite‐induced release of chemokine ligand CCL20 by airway epithelium

Post, S.; Rozeveld, Dennie; Jonker, Marnix; Bischoff, Rainer; Oosterhout, Antoon J. van; Heijink, Irene H.

doi:10.1111/all.12730

Cited by 17 publications

(21 citation statements)

References 36 publications

(45 reference statements)

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“…In addition, our laboratory has demonstrated that the HDM-induced ER stress is linked to increased CCL20 and IL-6 in wild-type mice (23). Furthermore, the proinflammatory cytokines (IL-6), Th2 cytokines (IL-13 and IL-4), Th17 cytokines (IL-17A), and chemokines, including CCL20, KC, and G-CSF, have been shown to play a critical role in the pathogenesis of allergic airway disease (1,7,18,47,48,64). In this study, TUDCA significantly decreased HDMinduced inflammatory cells in BALF and also significantly decreased IL-13, IL-4, IL-17A, IL-6, CCL20, KC, and G-CSF levels in HDM-challenged mice, either during the preventive regimen or rechallenge regimen.…”

Section: Discussionmentioning

confidence: 95%

“…Therefore, any effect of TUDCA on epithelial integrity is likely to protect against the extent of airway smooth muscle activation and thus central airway resistance. Additionally, TUDCA attenuated the HDM-induced increases in the levels of IL-13, IL-4, IL-17A, IL-6, and chemokines that play crucial roles in asthma pathophysiology (1,7,18,(47)(48)(49)64). Henceforth, we speculate that the protective effect of TUDCA on central airway resistance might be mediated through its effect on inflammatory cytokines/chemokines.…”

Section: Discussionmentioning

confidence: 99%

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Effect of a chemical chaperone, tauroursodeoxycholic acid, on HDM-induced allergic airway disease

Siddesha

Nakada

Mihavics

et al. 2016

American Journal of Physiology-Lung Cellular and Molecular Phys

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Endoplasmic reticulum (ER) stress-induced unfolded protein response plays a critical role in inflammatory diseases, including allergic airway disease. However, the benefits of inhibiting ER stress in the treatment of allergic airway disease are not well known. Herein, we tested the therapeutic potential of a chemical chaperone, tauroursodeoxycholic acid (TUDCA), in combating allergic asthma, using a mouse model of house dust mite (HDM)-induced allergic airway disease. TUDCA was administered during the HDM-challenge phase (preventive regimen), after the HDM-challenge phase (therapeutic regimen), or therapeutically during a subsequent HDM rechallenge (rechallenge regimen). In the preventive regimen, TUDCA significantly decreased HDM-induced inflammation, markers of ER stress, airway hyperresponsiveness (AHR), and fibrosis. Similarly, in the therapeutic regimen, TUDCA administration efficiently decreased HDM-induced airway inflammation, mucus metaplasia, ER stress markers, and AHR, but not airway remodeling. Interestingly, TUDCA administered therapeutically in the HDM rechallenge regimen markedly attenuated HDM-induced airway inflammation, mucus metaplasia, ER stress markers, methacholine-induced AHR, and airway fibrotic remodeling. These results indicate that the inhibition of ER stress in the lungs through the administration of chemical chaperones could be a valuable strategy in the treatment of allergic airway diseases.

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Section: Discussionmentioning

confidence: 95%

Section: Discussionmentioning

confidence: 99%

Effect of a chemical chaperone, tauroursodeoxycholic acid, on HDM-induced allergic airway disease

Siddesha

Nakada

Mihavics

et al. 2016

American Journal of Physiology-Lung Cellular and Molecular Phys

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“…The airway epithelium could function as a critical immune regulator through secretion of chemokines, cytokines, growth factors, and antimicrobial peptides. In this regard, the epithelial cells produce IL‐23, IL‐33, and thymic stromal lymphopoietin (TSLP), as well as CC family chemokines, which are regarded as critical epithelial factors to initiate and amplify airway inflammation . These newly identified epithelial‐specific cytokines are produced prior to the release of the more commonly recognized Th2‐type allergic inflammation mediators, including IL‐4, IL‐5, and IL‐13.…”

Section: Introductionmentioning

confidence: 99%

ITGB4is essential for containing HDM-induced airway inflammation and airway hyperresponsiveness

Liu

Lin

Zou

et al. 2018

Journal of Leukocyte Biology

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Airway epithelial cells play a significant role in the pathogenesis of asthma. Although the structural and functional defects of airway epithelial cells have been postulated to increase asthma susceptibility and exacerbate asthma severity, the mechanism and implication of these defects remain uncertain. Integrin β4 (ITGB4) is a structural adhesion molecule that is downregulated in the airway epithelium of asthma patients. In this study, we demonstrated that ITGB4 deficiency leads to severe allergy-induced airway inflammation and airway hyper-responsiveness (AHR) in mice. After house dust mite (HDM) challenge, epithelial cell-specific ITGB4-deleted mice showed increased lymphocyte, eosinophil, and neutrophil infiltration into lung compared with that of the wild-type mice. ITGB4 deficiency also resulted in increased expression of the Th2 cytokine IL-4, IL-13, and the Th17 cytokine IL-17A in the lung tissue and in the T cells after HDM challenge. The aggravated inflammation in ITGB4 defect mice was partly caused by enhanced disrupted epithelial barrier integrity after HDM stress, which induced the increased thymic stromal lymphopoietin secretion from airway epithelial cells. This study therefore demonstrates that ITGB4 plays a pivotal role in containing allergen-mediated lung inflammation and airway hyper-responsiveness in allergic asthma.

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“…Illustratively, ADAM 10 drives T H 2 bias 4 and promotes IgE synthesis by being a CD23 sheddase, 5 an effect incidentally ascribed to Der p 1 itself 3 . In airway epithelial cells, ADAM 10 liberates CCL20 (which recruits dendritic cells and T H 17 cells and promotes mucus hyperplasia), CCL2 (chemoattractant for dendritic cells), CCL5 (eosinophil chemokine), CXCL8 (neutrophil chemokine), and CXCL16 (T-cell chemoattractant) 6, 7. It is also involved in stem cell factor-dependent mast cell migration.…”

mentioning

confidence: 99%

Allergen-dependent oxidant formation requires purinoceptor activation of ADAM 10 and prothrombin

Chen

Zhang

Tachie-Menson

et al. 2017

Journal of Allergy and Clinical Immunology

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ADAM10 mediates the house dust mite‐induced release of chemokine ligand CCL20 by airway epithelium

Abstract: Our data show for the first time that ADAM10 activity contributes to HDM-induced shedding of chemokines, including CCL20. The ADAM10/CCL20 axis may be a target for novel therapeutic strategies in asthma.

Cited by 17 publications

References 36 publications

Effect of a chemical chaperone, tauroursodeoxycholic acid, on HDM-induced allergic airway disease

Effect of a chemical chaperone, tauroursodeoxycholic acid, on HDM-induced allergic airway disease

ITGB4is essential for containing HDM-induced airway inflammation and airway hyperresponsiveness

Allergen-dependent oxidant formation requires purinoceptor activation of ADAM 10 and prothrombin

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