دورية أكاديمية
Rhinovirus infection induces secretion of endothelin-1 from airway epithelial cells in both in vitro and in vivo models.
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.) |
References: | Compr Physiol. 2020 Jul 8;10(3):975-1007. (PMID: 32941682) Mucosal Immunol. 2010 Jan;3(1):69-80. (PMID: 19710636) Am J Respir Cell Mol Biol. 2016 Apr;54(4):524-31. (PMID: 26407210) Nat Med. 2013 Feb;19(2):232-7. (PMID: 23334847) Sci Rep. 2021 Aug 10;11(1):16212. (PMID: 34376762) Nat Med. 2008 Feb;14(2):199-204. (PMID: 18246079) Nat Commun. 2020 Oct 7;11(1):5053. (PMID: 33028821) Methods. 2001 Dec;25(4):402-8. (PMID: 11846609) J Allergy Clin Immunol. 1995 Nov;96(5 Pt 1):618-27. (PMID: 7499678) Am J Respir Cell Mol Biol. 2016 May;54(5):647-55. (PMID: 26796672) J Allergy Clin Immunol. 2018 May;141(5):1887-1890.e1. (PMID: 29317243) PLoS Pathog. 2017 Jan 3;13(1):e1006138. (PMID: 28046097) Nat Rev Immunol. 2014 Oct;14(10):686-98. (PMID: 25234144) Am J Respir Cell Mol Biol. 2007 Jul;37(1):38-47. (PMID: 17379848) Methods Mol Biol. 2015;1221:49-61. (PMID: 25261306) Thorax. 2015 Sep;70(9):854-61. (PMID: 26108570) Expert Rev Respir Med. 2016 Jun;10(6):629-41. (PMID: 27088397) Hypertension. 2019 Dec;74(6):1232-1265. (PMID: 31679425) N Engl J Med. 2017 Sep 7;377(10):965-976. (PMID: 28877019) FASEB J. 2011 Jan;25(1):16-28. (PMID: 20837776) Am J Physiol Lung Cell Mol Physiol. 2021 Feb 1;320(2):L246-L253. (PMID: 33174447) Ann Allergy. 1994 Oct;73(4):365-9. (PMID: 7944006) Commun Biol. 2022 May 4;5(1):415. (PMID: 35508632) J Allergy Clin Immunol. 2007 Dec;120(6):1301-7. (PMID: 17996929) Front Cell Infect Microbiol. 2020 Aug 31;10:456. (PMID: 32984077) Am J Respir Crit Care Med. 1997 Aug;156(2 Pt 1):591-9. (PMID: 9279245) Am J Respir Cell Mol Biol. 2003 Feb;28(2):142-9. (PMID: 12540481) Respir Res. 2000;1(1):54-61. (PMID: 11667966) Am J Physiol Lung Cell Mol Physiol. 2017 Jan 1;312(1):L89-L99. (PMID: 27836899) Respir Res. 2018 Oct 29;19(1):208. (PMID: 30373568) Ann Allergy Asthma Immunol. 2019 Oct;123(4):352-358. (PMID: 31276807) Sci Rep. 2020 Jan 22;10(1):966. (PMID: 31969610) Nat Med. 2012 May 04;18(5):684-92. (PMID: 22561832) Virology. 2013 Feb 5;436(1):143-9. (PMID: 23199420) J Allergy Clin Immunol. 2014 Jun;133(6):1720-7. (PMID: 24388637) PLoS Pathog. 2010 Nov 04;6(11):e1001178. (PMID: 21079690) Am J Respir Crit Care Med. 1997 Aug;156(2 Pt 1):642-7. (PMID: 9279252) Nature. 1988 Mar 31;332(6163):411-5. (PMID: 2451132) Am J Respir Cell Mol Biol. 2006 Dec;35(6):628-38. (PMID: 16794260) Respir Res. 2001;2(2):90-101. (PMID: 11686871) Am J Respir Cell Mol Biol. 2009 Oct;41(4):459-66. (PMID: 19168703) Am J Respir Cell Mol Biol. 2017 Apr;56(4):432-442. (PMID: 27854509) J Virol Methods. 2015 Jun 1;217:18-23. (PMID: 25724434) Am J Physiol Lung Cell Mol Physiol. 2018 Nov 1;315(5):L645-L652. (PMID: 30070589) PLoS One. 2012;7(9):e44580. (PMID: 22970254) Allergy. 2013 Dec;68(12):1579-88. (PMID: 24117726) J Gen Virol. 2011 Nov;92(Pt 11):2549-2557. (PMID: 21752966) Am J Respir Crit Care Med. 1997 Aug;156(2 Pt 1):600-8. (PMID: 9279246) Am J Respir Crit Care Med. 1997 Aug;156(2 Pt 1):382-8. (PMID: 9279213) J Allergy Clin Immunol. 1991 Sep;88(3 Pt 1):376-84. (PMID: 1890266) Am J Respir Crit Care Med. 2008 Oct 1;178(7):667-72. (PMID: 18565953) Nat Rev Immunol. 2002 Feb;2(2):132-8. (PMID: 11910895) J Allergy Clin Immunol. 2017 Oct;140(4):895-906. (PMID: 28987219) Am J Physiol Lung Cell Mol Physiol. 2023 Aug 1;325(2):L206-L214. (PMID: 37280545) |
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 |
تدمد: | 1465-993X |
---|---|
DOI: | 10.1186/s12931-023-02510-6 |