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.

Nasal epithelial cells express IL-10 at levels that negatively correlate with clinical symptoms in patients with house dust mite allergy

Allergy ◽  
2007 ◽  
Vol 62 (9) ◽  
pp. 1014-1022 ◽  
Author(s):  
B. Muller ◽  
E. J. J. de Groot ◽  
I. J. M. Kortekaas ◽  
W. J. Fokkens ◽  
C. M. van Drunen
Keyword(s):  
Epithelial Cells ◽  
House Dust ◽  
House Dust Mite ◽  
Clinical Symptoms ◽  
Nasal Epithelial Cells ◽  
House Dust Mite Allergy ◽  
Mite Allergy ◽  
Dust Mite

scholarly journals Elovanoid 34 Reduces Proinflammatory Cytokines and Arrest the Expression of Genes That Drive Senescence, Autophagy, Unfolded Protein Response (UPR), Matrix Metalloproteinases (MMPs) and Inflammation in Human Nasal Cells Exposed to House Dust Mite (HDM): Therapeutic Potential in Allergy

2021 ◽  
Author(s):  
Alfredo Resano ◽  
Miguel Barajas ◽  
Surjyadipta Bhattacharjee ◽  
Roberto Aguado-Jiménez ◽  
David Rodríguez ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Matrix Metalloproteinases ◽  
Unfolded Protein Response ◽  
House Dust ◽  
House Dust Mite ◽  
Permeability Barrier ◽  
Nasal Epithelial Cells ◽  
Unfolded Protein ◽  
Dust Mite ◽  
Protein Response

Elovanoids (ELV) are novel lipid mediators synthesized from very long-chain (VLC) omega-3 (n-3) polyunsaturated fatty acids (PUFA), particularly docosahexaenoic acid (DHA) or eicosa-pentaenoic acid (EPA), by the elongase enzyme ELOVL4. ELV have been shown to play a funda-mental role in maintaining brain and retina function, neuroprotection, maintaining the skin's permeability barrier, and sperm function, among other important cellular processes. Furthermore, the methyl ester or sodium salt of ELV-N32 and ELV-N34 have been found to be efficient in re-duced infarct volumes, promoting cell survival and decreasing the alteration of the neurovascular unit in a model of ischemia due to occlusion of the middle cerebral artery. Their bioactivity in-cludes enhancing of anti-apoptotic and pro-survival protein expression combined with the downregulation of pro-apoptotic proteins. House dust mite (HDM) is the most prevalent indoor allergen, and HDM exposure is frequently the cause of allergic respiratory disease, including aller-gic rhinitis and allergic asthma in HDM sensitized individuals. In our study, human nasal epithe-lial cells (HNEpC) were used as an in vitro model for allergy. The cells were challenged with HDM (mixture of Dermatophagoides farinae and D. pteronyssinus extract), with or without treat-ment with ELV-34. Phosphate-buffered saline (PBS) (vehicle) and ELV-34 (500 nM) alone were used as the control. Our findings show that ELV-34 promotes cell viability and reduces cytotoxi-city upon HDM sensitization of HNEpC. ELV-34 treatment significantly reduces the levels of IL-6, IL-1β, IL-8, VEGF, ICAM1, CXCL1 and CCL2, restored the IL-10 level and diminishes the induc-tion of the transcription of inflammatory and senescence genes in HNEpC. Our data also shows that HDM triggered the expression of several key genes in human nasal epithelial cells, including autophagy, unfolded protein response (UPR), Matrix metalloproteinases (MMPs), senescence and inflammation markers. Together, our data reveal a novel pro-homeostatic and cell-protective li-pid-signaling mechanism in nasal epithelial cells that envision novel potential therapeutic targets for the treatment of allergies.

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