دورية أكاديمية
أعرض في EDS

Infection of Endothelial Cells by Dengue Virus Induces ROS Production by Different Sources Affecting Virus Replication, Cellular Activation, Death and Vascular Permeability.

التفاصيل البيبلوغرافية
العنوان: Infection of Endothelial Cells by Dengue Virus Induces ROS Production by Different Sources Affecting Virus Replication, Cellular Activation, Death and Vascular Permeability.
المؤلفون: Meuren LM; Departamento de Virologia, Instituto de Microbiologia Paulo de Góes, Universidade Federal do Rio de Janeiro, Rio de Janeiro, Brazil., Prestes EB; Laboratório de Inflamação e Imunidade, Departamento de Imunologia, Instituto de Microbiologia Paulo de Góes, Universidade Federal do Rio de Janeiro, Rio de Janeiro, Brazil., Papa MP; Departamento de Virologia, Instituto de Microbiologia Paulo de Góes, Universidade Federal do Rio de Janeiro, Rio de Janeiro, Brazil.; Department of Microbiology, Immunology and Tropical Medicine, The George Washington University, Washington, DC, United States., de Carvalho LRP; Instituto de Bioquímica Médica Leopoldo de Meis, Universidade Federal do Rio de Janeiro, Rio de Janeiro, Brazil., Mustafá YM; Departamento de Virologia, Instituto de Microbiologia Paulo de Góes, Universidade Federal do Rio de Janeiro, Rio de Janeiro, Brazil., da Costa LS; Instituto de Bioquímica Médica Leopoldo de Meis, Universidade Federal do Rio de Janeiro, Rio de Janeiro, Brazil., Da Poian AT; Instituto de Bioquímica Médica Leopoldo de Meis, Universidade Federal do Rio de Janeiro, Rio de Janeiro, Brazil., Bozza MT; Laboratório de Inflamação e Imunidade, Departamento de Imunologia, Instituto de Microbiologia Paulo de Góes, Universidade Federal do Rio de Janeiro, Rio de Janeiro, Brazil., Arruda LB; Departamento de Virologia, Instituto de Microbiologia Paulo de Góes, Universidade Federal do Rio de Janeiro, Rio de Janeiro, Brazil.
المصدر: Frontiers in immunology [Front Immunol] 2022 Feb 02; Vol. 13, pp. 810376. Date of Electronic Publication: 2022 Feb 02 (Print Publication: 2022).
نوع المنشور: Journal Article; Research Support, Non-U.S. Gov't
اللغة: English
بيانات الدورية: Publisher: Frontiers Research Foundation] Country of Publication: Switzerland NLM ID: 101560960 Publication Model: eCollection Cited Medium: Internet ISSN: 1664-3224 (Electronic) Linking ISSN: 16643224 NLM ISO Abbreviation: Front Immunol Subsets: MEDLINE
أسماء مطبوعة: Original Publication: [Lausanne : Frontiers Research Foundation]
مواضيع طبية MeSH: Antiviral Agents/*pharmacology , Dengue Virus/*drug effects , Endothelium, Vascular/*virology , Reactive Oxygen Species/*metabolism , Virus Replication/*drug effects, Capillary Permeability/drug effects ; Cell Line ; Cells, Cultured ; Cytokines/metabolism ; Dengue/immunology ; Dengue/virology ; Dengue Virus/genetics ; Endothelium, Vascular/drug effects ; Humans ; Oxidative Stress/drug effects
مستخلص: Exacerbated inflammatory response and altered vascular function are hallmarks of dengue disease. Reactive oxygen species (ROS) production has been associated to endothelial barrier disturbance and microvascular alteration in distinct pathological conditions. Increased ROS has been reported in in vitro models of dengue virus (DENV) infection, but its impact for endothelial cell physiology had not been fully investigated. Our group had previously demonstrated that infection of human brain microvascular endothelial cells (HBMEC) with DENV results in the activation of RNA sensors and production of proinflammatory cytokines, which culminate in cell death and endothelial permeability. Here, we evaluated the role of mitochondrial function and NADPH oxidase (NOX) activation for ROS generation in HBMEC infected by DENV and investigated whether altered cellular physiology could be a consequence of virus-induced oxidative stress. DENV-infected HBMECs showed a decrease in the maximal respiratory capacity and altered membrane potential, indicating functional mitochondrial alteration, what might be related to mtROS production. Indeed, mtROS was detected at later time points after infection. Specific inhibition of mtROS diminished virus replication, cell death, and endothelial permeability, but did not affect cytokine production. On the other hand, inhibition of NOX-associated ROS production decreased virus replication and cell death, as well as the secretion of inflammatory cytokines, including IL-6, IL-8, and CCL5. These results demonstrated that DENV replication in endothelial cells induces ROS production by different pathways, which impacts biological functions that might be relevant for dengue pathogenesis. Those data also indicate oxidative stress events as relevant therapeutical targets to avoid vascular permeability, inflammation, and neuroinvasion during DENV infection.
Competing Interests: The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.
(Copyright © 2022 Meuren, Prestes, Papa, de Carvalho, Mustafá, da Costa, Da Poian, Bozza and Arruda.)
References: J Clin Invest. 2006 Oct;116(10):2739-47. (PMID: 16998589)
Viruses. 2019 May 10;11(5):. (PMID: 31083280)
Front Physiol. 2020 May 27;11:472. (PMID: 32536875)
PLoS One. 2013 Aug 28;8(8):e74035. (PMID: 24015314)
Cells. 2019 Nov 11;8(11):. (PMID: 31717900)
Biochim Biophys Acta. 2007 Oct;1772(10):1158-66. (PMID: 17964123)
PLoS One. 2012;7(4):e33871. (PMID: 22485151)
Brain. 2006 Jan;129(Pt 1):212-23. (PMID: 16230319)
Clin Microbiol Rev. 2009 Oct;22(4):564-81. (PMID: 19822889)
J Virol. 2020 Nov 23;94(24):. (PMID: 32999020)
Gastroenterology. 2002 Feb;122(2):366-75. (PMID: 11832451)
Immunology. 2017 Jul;151(3):261-269. (PMID: 28437586)
Hypertension. 2008 Feb;51(2):211-7. (PMID: 18086956)
Virology. 2001 Sep 15;288(1):1-7. (PMID: 11543652)
Int J Infect Dis. 2014 Jan;18:68-72. (PMID: 24216294)
Int J Cell Biol. 2014;2014:467452. (PMID: 24899897)
Free Radic Biol Med. 2012 Sep 15;53(6):1213-21. (PMID: 22796592)
Annu Rev Pathol. 2013 Jan 24;8:411-40. (PMID: 23121052)
Endothelium. 2002;9(3):191-203. (PMID: 12380644)
Mol Cell Neurosci. 2014 Jul;61:72-84. (PMID: 24907586)
Viruses. 2020 Mar 24;12(3):. (PMID: 32213866)
Cells. 2020 Aug 06;9(8):. (PMID: 32781794)
Clin Infect Dis. 2017 Oct 16;65(9):1453-1461. (PMID: 28673038)
J Biol Chem. 2011 Jun 24;286(25):22147-59. (PMID: 21511946)
Physiol Rev. 2014 Jul;94(3):909-50. (PMID: 24987008)
J Gen Virol. 2021 Apr;102(4):. (PMID: 33904816)
Biochim Biophys Acta. 2006 Sep-Oct;1757(9-10):1429-37. (PMID: 16814246)
Front Microbiol. 2017 Dec 22;8:2557. (PMID: 29312238)
Ann N Y Acad Sci. 2009 Sep;1171 Suppl 1:E42-7. (PMID: 19751401)
FEMS Immunol Med Microbiol. 2008 Aug;53(3):287-99. (PMID: 18522648)
Cell Death Dis. 2016 Mar 03;7:e2127. (PMID: 26938301)
J Virol. 2008 Dec;82(24):12312-24. (PMID: 18842737)
Nat Microbiol. 2020 Jun;5(6):796-812. (PMID: 32367055)
Sci Signal. 2016 Nov 29;9(456):ra115. (PMID: 27899525)
J Lab Autom. 2015 Apr;20(2):107-26. (PMID: 25586998)
Pharmaceuticals (Basel). 2021 Jan 12;14(1):. (PMID: 33445640)
Open Biol. 2019 Mar 29;9(3):190009. (PMID: 30862253)
Arterioscler Thromb Vasc Biol. 2005 Jan;25(1):29-38. (PMID: 15539615)
Cell Host Microbe. 2016 Sep 14;20(3):342-356. (PMID: 27545046)
Methods. 2001 Dec;25(4):402-8. (PMID: 11846609)
Acta Trop. 2008 Jun;106(3):156-61. (PMID: 18420173)
Blood. 2012 Mar 8;119(10):2368-75. (PMID: 22262768)
PLoS One. 2014 Apr 15;9(4):e83386. (PMID: 24736395)
J Physiol. 2003 Oct 15;552(Pt 2):335-44. (PMID: 14561818)
Viral Immunol. 2020 Jan/Feb;33(1):61-70. (PMID: 31978319)
Virology. 2013 Jan 20;435(2):281-92. (PMID: 23089253)
Curr Cardiol Rev. 2018;14(4):290-300. (PMID: 29962348)
Elife. 2019 Jun 27;8:. (PMID: 31246170)
Exp Mol Pathol. 2014 Dec;97(3):386-92. (PMID: 25220346)
Arch Virol. 2019 Dec;164(12):2895-2908. (PMID: 31531742)
Antioxid Redox Signal. 2014 Mar 1;20(7):1126-67. (PMID: 23991888)
J Virol Methods. 2010 Jan;163(1):1-9. (PMID: 19822173)
PLoS Pathog. 2014 Dec 18;10(12):e1004566. (PMID: 25521078)
J Cell Sci. 2019 Apr 26;132(8):. (PMID: 31028152)
Front Microbiol. 2016 Aug 25;7:1233. (PMID: 27610098)
Viruses. 2020 Aug 25;12(9):. (PMID: 32854254)
J Virol. 2000 Sep;74(18):8680-91. (PMID: 10954569)
Cell Host Microbe. 2010 Feb 18;7(2):128-39. (PMID: 20153282)
Free Radic Biol Med. 2012 Jan 1;52(1):1-6. (PMID: 22027063)
Front Endocrinol (Lausanne). 2020 Sep 23;11:568305. (PMID: 33071976)
J Virol. 2010 Mar;84(5):2421-31. (PMID: 20032188)
فهرسة مساهمة: Keywords: NADPH oxidase; cell death; cytokines; dengue; human brain microvascular endothelial cells (HBMEC); mitochondria; reactive oxygen species
المشرفين على المادة: 0 (Antiviral Agents)
0 (Cytokines)
0 (Reactive Oxygen Species)
تواريخ الأحداث: Date Created: 20220221 Date Completed: 20220328 Latest Revision: 20220328
رمز التحديث: 20231215
مُعرف محوري في PubMed: PMC8847576
DOI: 10.3389/fimmu.2022.810376
PMID: 35185902
قاعدة البيانات: MEDLINE
الوصف
تدمد:1664-3224
DOI:10.3389/fimmu.2022.810376