TRPV4-Mediated Epithelial Junction Disruption in Allergic Rhinitis Triggered by House Dust Mites

2020 ◽  
pp. 194589242096416
Author(s):  
Kijeong Lee ◽  
Junhyoung Byun ◽  
Byoungjae Kim ◽  
Jiwoo Yeon ◽  
Junhu Tai ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
House Dust ◽  
Nasal Epithelial Cells ◽  
Zonula Occludens ◽  
Dust Mite ◽  
Cultured Epithelial Cells ◽  
Junctional Protein ◽  
Der P 1 ◽  
Zonula Occludens 1

Background Epithelial barrier disruption is a crucial feature of allergic rhinitis (AR). Previous reports have indicated the role of transient receptor potential vanilloid (TRPV) 4 in regulating the intercellular junctions in various cells. However, the role of TRPV4 and its regulation by T helper 2 cell cytokines in the epithelial cells of patients with AR remains unclear. Objective We aimed to elucidate the expression of TRPV4 in nasal epithelial cells and its cytokine-induced regulation, and to reveal its role in house dust mite-induced junction disruption in AR. Methods The expression of TRPV4 in nasal epithelial cells was measured using real-time polymerase chain reaction, western blot, and immunohistochemical assays, and the expression levels were compared between the patients with AR and healthy controls. Altered expression of TRPV4 was induced in cultured nasal epithelial cells by stimulation of interleukin (IL) 4, IL-13, and tumor necrosis factor alpha. In addition, expression of E-cadherin and zonula occludens 1 was induced in Der p 1-stimulated epithelial cells by treatment with either a TRPV4 agonist (GSK1016790A) or a TRPV4 antagonist (RN1734). Results TRPV4 expression was increased in epithelial cells harvested from the affected turbinates compared to those from the normal turbinates. The stimulation of cultured epithelial cells with IL-4 and IL-13 resulted in TRPV4 upregulation. Additionally, E-cadherin and zonula occludens 1 expression levels decreased in the cultured epithelial cells treated with GSK1016790A after stimulation with Der p 1, whereas Der p 1 stimulation alone showed no effect on junctional protein expression. Conclusions Increased TRPV4 expression occurred in epithelial cells harvested from patients with AR and epithelial cells stimulated by Th2 cytokines. Decreased junctional protein expression in epithelial cells after the stimulation by house dust mite allergen with TRPV4 agonist indicates a possible role of TRPV4 in the pathogenesis of allergen-induced epithelial barrier disruption in AR.

scholarly journals Helicobacter pylori–induced matrix metallopeptidase-10 promotes gastric bacterial colonization and gastritis

2019 ◽  
Vol 5 (4) ◽  
pp. eaau6547 ◽  
Author(s):  
Yi-pin Lv ◽  
Ping Cheng ◽  
Jin-yu Zhang ◽  
Fang-yuan Mao ◽  
Yong-sheng Teng ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Bacterial Colonization ◽  
Gastric Epithelium ◽  
Erk Pathway ◽  
Gastric Epithelial Cells ◽  
Zonula Occludens ◽  
Matrix Metallopeptidase ◽  
Zonula Occludens 1 ◽  
H Pylori

The interaction between gastric epithelium and immune response plays key roles in H. pylori–associated pathology. We demonstrated a procolonization and proinflammation role of MMP-10 in H. pylori infection. MMP-10 is elevated in gastric mucosa and is produced by gastric epithelial cells synergistically induced by H. pylori and IL-22 via the ERK pathway. Human gastric MMP-10 was correlated with H. pylori colonization and the severity of gastritis, and mouse MMP-10 from non–BM-derived cells promoted bacteria colonization and inflammation. H. pylori colonization and inflammation were attenuated in IL-22−/−, MMP-10−/−, and IL-22−/−MMP-10−/− mice. MMP-10–associated inflammation is characterized by the influx of CD8+ T cells, whose migration is induced via MMP-10–CXCL16 axis by gastric epithelial cells. Under the influence of MMP-10, Reg3a, E-cadherin, and zonula occludens–1 proteins decrease, resulting in impaired host defense and increased H. pylori colonization. Our results suggest that MMP-10 facilitates H. pylori persistence and promotes gastritis.

Role of Der p 1–specific B cells in immune tolerance during 2 years of house dust mite–specific immunotherapy

2019 ◽  
Vol 143 (3) ◽  
pp. 1077-1086.e10 ◽  
Author(s):  
Tadech Boonpiyathad ◽  
Willem van de Veen ◽  
Oliver Wirz ◽  
Milena Sokolowska ◽  
Beate Rückert ◽  
...  
Keyword(s):  
B Cells ◽  
Immune Tolerance ◽  
House Dust ◽  
House Dust Mite ◽  
Specific Immunotherapy ◽  
Dust Mite ◽  
Der P 1

scholarly journals Evaluation of the Role of IgE Responses to Der p 1 and Der p 2 in Chinese House Dust Mite-Allergic Patients

2015 ◽  
Vol 167 (3) ◽  
pp. 203-210 ◽  
Author(s):  
Hui-Ying Wang ◽  
Zhong-Shan Gao ◽  
Xiang Zhou ◽  
Yu Dai ◽  
Wo Yao ◽  
...  
Keyword(s):  
House Dust ◽  
House Dust Mite ◽  
Dust Mite ◽  
Der P 1 ◽  
Der P 2

scholarly journals Impaired barrier function in patients with house dust mite–induced allergic rhinitis is accompanied by decreased occludin and zonula occludens-1 expression

2016 ◽  
Vol 137 (4) ◽  
pp. 1043-1053.e5 ◽  
Author(s):  
Brecht Steelant ◽  
Ricard Farré ◽  
Paulina Wawrzyniak ◽  
Jochen Belmans ◽  
Emily Dekimpe ◽  
...  
Keyword(s):  
Allergic Rhinitis ◽  
House Dust ◽  
House Dust Mite ◽  
Barrier Function ◽  
Zonula Occludens ◽  
Dust Mite ◽  
Zonula Occludens 1

scholarly journals House Dust Mite Induces IL-33 Release From Human Nasal Epithelial Cells via P2Y Purinergic Signals and ERK/P38 MAPK Pathways.

2021 ◽  
Author(s):  
Bin Liu ◽  
Pei Zhou ◽  
Tingting Feng ◽  
Jiping Li
Keyword(s):  
Epithelial Cells ◽  
House Dust ◽  
House Dust Mite ◽  
Atp Release ◽  
Extracellular Atp ◽  
Nasal Epithelial Cells ◽  
Interleukin 33 ◽  
Atp Assay ◽  
Human Nasal Epithelial Cells ◽  
Dust Mite

Abstract BackgroundAllergic rhinitis (AR) is an inflammatory disease of the nasal mucosa, which is triggered by stimulations of environmental allergens such as house dust mite (HDM). Th2-type proinflammatory factor interleukin 33 (IL-33) plays an important role in the pathogenesis of AR, but it remains unknown how IL-33 products in human nasal epithelial cells (HNECs) mediated by HDM. MethodsWe investigated the effect of HDM allergens by analyzing the accumulation of Ca2+ levels and IL-33 release in HNECs. Involvements of Adenosine triphosphate (ATP)-dependent activation of P2Y-PLC-IP3 pathways, downstream of Ca2+ signaling and P38/ERK pathways were studied, using the P2Y-PLC-IP3 pathways agonists, the calcium chelators, and P38/ERK pathways inhibitors. ResultsDer p induced expression of IL-33 mRNA and protein in HNECs via ERK/P38 pathways. Average 69.4% of co-localization of quinacrine and Lyso-tracker fluorescent puncta revealed that ATP was mainly stored in the lysosomes of nasal epithelial cells. After stimulation with Der p, ATP released from lysosomes by P2Y-PLC-IP3-Ca2+pathways. The ATP assay of HNECs culture supernatants implied an acute accumulation of extracellular ATP immediately after the Der p stimulation. Using P2Y-PLC-IP3 signaling inhibitors, we found that the Der p-induced IL-33 release was dependent on ATP-P2Y-PLC-IP3 signaling, followed by abolishing the ERK/P38 pathways. ConclusionDer p induced an acute accumulation of extracellular ATP which activated PY2-PLC-IP3 pathways to induce Ca2+ releasing from endoplasmic reticulum (ER), and intracellular Ca2+ induced ATP release from lysosomes from HNECs. ATP activated PY2-PLC-IP3 pathways followed by transactivation of ERK/P38 pathways which induced the expression of IL-33 mRNA and protein.

scholarly journals House Dust Mite Exposure Causes Increased Susceptibility of Nasal Epithelial Cells to Adenovirus Infection

Viruses ◽  
2020 ◽  
Vol 12 (10) ◽  
pp. 1151
Author(s):  
Malik Aydin ◽  
Ella A. Naumova ◽  
Friedrich Paulsen ◽  
Wenli Zhang ◽  
Felix Gopon ◽  
...  
Keyword(s):  
Cell Culture ◽  
Epithelial Cells ◽  
House Dust ◽  
House Dust Mite ◽  
Fluorescent Protein ◽  
Ex Vivo ◽  
Study Cohort ◽  
Nasal Epithelial Cells ◽  
Dust Mite ◽  
The Impact

Adenovirus (AdV) infections in the respiratory tract may cause asthma exacerbation and allergic predisposition, and the house dust mite (HDM) may aggravate virus-induced asthma exacerbations. However, the underlying mechanisms of whether and how AdV affects asthmatic patients remains unclear. To address this question, we investigated nasal epithelial cells (NAEPCs) derived from a pediatric exacerbation study cohort for experimental analyses. We analyzed twenty-one different green-fluorescent protein- and luciferase-tagged AdV types in submerged 2D and organotypic 3D cell culture models. Transduction experiments revealed robust transduction of AdV type 5 (AdV5) in NAEPCs, which was associated with an increased uptake of AdV5 in the presence of HDM. In healthy and asthmatic NAEPCs exposed to HDM before infection, we observed a time- and dose-dependent increase of AdV5 uptake associated with upregulation of entry receptors for AdV5. Furthermore, electron microscopic and histologic analyses of 3D cell cultures revealed an impairment of the respiratory cilia after HDM exposition. This ex vivo pilot study shows the impact of AdV infection and HDM exposition in a primary cell culture model for asthma.

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