دورية أكاديمية
أعرض في EDS

Rhinovirus infection induces secretion of endothelin-1 from airway epithelial cells in both in vitro and in vivo models.

التفاصيل البيبلوغرافية
العنوان: Rhinovirus infection induces secretion of endothelin-1 from airway epithelial cells in both in vitro and in vivo models.
المؤلفون: Dy ABC; Program in Molecular and Integrative Physiological Sciences, Department of Environmental Health, Harvard T.H. Chan School of Public Health, 665 Huntington Ave, Boston, MA, SPH1-315, USA., Girkin J; College of Health, Medicine and Wellbeing, University of Newcastle and Hunter Medical Research Institute, New Lambton Heights, Australia., Marrocco A; Program in Molecular and Integrative Physiological Sciences, Department of Environmental Health, Harvard T.H. Chan School of Public Health, 665 Huntington Ave, Boston, MA, SPH1-315, USA., Collison A; College of Health, Medicine and Wellbeing, University of Newcastle and Hunter Medical Research Institute, New Lambton Heights, Australia., Mwase C; Program in Molecular and Integrative Physiological Sciences, Department of Environmental Health, Harvard T.H. Chan School of Public Health, 665 Huntington Ave, Boston, MA, SPH1-315, USA., O'Sullivan MJ; Program in Molecular and Integrative Physiological Sciences, Department of Environmental Health, Harvard T.H. Chan School of Public Health, 665 Huntington Ave, Boston, MA, SPH1-315, USA., Phung TN; Program in Molecular and Integrative Physiological Sciences, Department of Environmental Health, Harvard T.H. Chan School of Public Health, 665 Huntington Ave, Boston, MA, SPH1-315, USA., Mattes J; College of Health, Medicine and Wellbeing, University of Newcastle and Hunter Medical Research Institute, New Lambton Heights, Australia., Koziol-White C; Robert Wood Johnson Medical School, Rutgers University, New Brunswick, NJ, USA., Gern JE; Department of Pediatrics, School of Medicine and Public Health, University of Wisconsin-Madison, Madison, WI, USA., Bochkov YA; Department of Pediatrics, School of Medicine and Public Health, University of Wisconsin-Madison, Madison, WI, USA., Bartlett NW; College of Health, Medicine and Wellbeing, University of Newcastle and Hunter Medical Research Institute, New Lambton Heights, Australia., Park JA; Program in Molecular and Integrative Physiological Sciences, Department of Environmental Health, Harvard T.H. Chan School of Public Health, 665 Huntington Ave, Boston, MA, SPH1-315, USA. jpark@hsph.harvard.edu.
المصدر: Respiratory research [Respir Res] 2023 Aug 19; Vol. 24 (1), pp. 205. Date of Electronic Publication: 2023 Aug 19.
نوع المنشور: Journal Article
اللغة: English
بيانات الدورية: Publisher: BioMed Central Ltd Country of Publication: England NLM ID: 101090633 Publication Model: Electronic Cited Medium: Internet ISSN: 1465-993X (Electronic) Linking ISSN: 14659921 NLM ISO Abbreviation: Respir Res Subsets: MEDLINE
أسماء مطبوعة: Publication: 2001- : London : BioMed Central Ltd.
Original Publication: London : Current Science Ltd., c2000-
مواضيع طبية MeSH: Hypersensitivity* , Asthma*/chemically induced, Humans ; Animals ; Mice ; Endothelin-1 ; Rhinovirus ; Toll-Like Receptor 3 ; Receptors, Transforming Growth Factor beta
مستخلص: Background: Rhinovirus (RV) infection of airway epithelial cells triggers asthma exacerbations, during which airway smooth muscle (ASM) excessively contracts. Due to ASM contraction, airway epithelial cells become mechanically compressed. We previously reported that compressed human bronchial epithelial (HBE) cells are a source of endothelin-1 (ET-1) that causes ASM contraction. Here, we hypothesized that epithelial sensing of RV by TLR3 and epithelial compression induce ET-1 secretion through a TGF-β receptor (TGFβR)-dependent mechanism.
Methods: To test this, we used primary HBE cells well-differentiated in air-liquid interface culture and two mouse models (ovalbumin and house dust mite) of allergic airway disease (AAD). HBE cells were infected with RV-A16, treated with a TLR3 agonist (poly(I:C)), or exposed to compression. Thereafter, EDN1 (ET-1 protein-encoding gene) mRNA expression and secreted ET-1 protein were measured. We examined the role of TGFβR in ET-1 secretion using either a pharmacologic inhibitor of TGFβR or recombinant TGF-β1 protein. In the AAD mouse models, allergen-sensitized and allergen-challenged mice were subsequently infected with RV. We then measured ET-1 in bronchoalveolar lavage fluid (BALF) and airway hyperresponsiveness (AHR) following methacholine challenge.
Results: Our data reveal that RV infection induced EDN1 expression and ET-1 secretion in HBE cells, potentially mediated by TLR3. TGFβR activation was partially required for ET-1 secretion, which was induced by RV, poly(I:C), or compression. TGFβR activation alone was sufficient to increase ET-1 secretion. In AAD mouse models, RV induced ET-1 secretion in BALF, which positively correlated with AHR.
Conclusions: Our data provide evidence that RV infection increased epithelial-cell ET-1 secretion through a TGFβR-dependent mechanism, which contributes to bronchoconstriction during RV-induced asthma exacerbations.
(© 2023. BioMed Central Ltd., part of Springer Nature.)
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معلومات مُعتمدة: R01HL148152 United States GF NIH HHS; R01 HL148152 United States HL NHLBI NIH HHS; R01 AI148707 United States AI NIAID NIH HHS; R56HL142890 United States GF NIH HHS; T32 HL007118 United States HL NHLBI NIH HHS; U19AI104317 United States GF NIH HHS
فهرسة مساهمة: Keywords: Asthma exacerbations; Bronchoconstriction; Epithelial endothelin-1; Mechanical compression; Rhinovirus infection
المشرفين على المادة: 0 (Endothelin-1)
0 (Toll-Like Receptor 3)
0 (Receptors, Transforming Growth Factor beta)
تواريخ الأحداث: Date Created: 20230819 Date Completed: 20230821 Latest Revision: 20240203
رمز التحديث: 20240205
مُعرف محوري في PubMed: PMC10440034
DOI: 10.1186/s12931-023-02510-6
PMID: 37598152
قاعدة البيانات: MEDLINE
الوصف
تدمد:1465-993X
DOI:10.1186/s12931-023-02510-6