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Anti-inflammatory actions of aspirin-triggered resolvin D1 (AT-RvD1) in bronchial epithelial cells stimulated by cigarette smoke extract
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  • Alexandre de Paula Rogério,
  • Jhony Robison de Oliveira,
  • Aline Beatriz Mahler Pereira,
  • Henrique Ismarsi Souza,
  • Wanessa Maria dos Santos,
  • Thaís Soares Farnesi de Assunção,
  • Paulo Roberto da Silva,
  • Marcos Vinícius Silva,
  • Virmondes Rodrigues Júnior
Alexandre de Paula Rogério
Universidade Federal do Triangulo Mineiro Faculdade de Medicina

Corresponding Author:[email protected]

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Jhony Robison de Oliveira
Universidade Federal do Triangulo Mineiro Faculdade de Medicina
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Aline Beatriz Mahler Pereira
Universidade Federal do Triangulo Mineiro Faculdade de Medicina
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Henrique Ismarsi Souza
Universidade Federal do Triangulo Mineiro Faculdade de Medicina
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Wanessa Maria dos Santos
Universidade Federal do Triangulo Mineiro Faculdade de Medicina
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Thaís Soares Farnesi de Assunção
Universidade Federal do Triangulo Mineiro Faculdade de Medicina
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Paulo Roberto da Silva
Universidade Federal do Triangulo Mineiro Faculdade de Medicina
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Marcos Vinícius Silva
Universidade Federal do Triangulo Mineiro Faculdade de Medicina
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Virmondes Rodrigues Júnior
Universidade Federal do Triangulo Mineiro Faculdade de Medicina
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Abstract

Smoking causes several diseases such as chronic obstructive pulmonary disease (COPD). Aspirin-triggered-resolvin D1 (AT-RvD1) is a lipid mediator produced during the resolution of inflammation and demonstrates anti-inflammatory and pro-resolution effects in several inflammatory experimental models including in the airways. Here we evaluated the role of AT-RvD1 (100nM) in bronchial epithelial cells (BEAS-2B) stimulated by cigarette smoke extract (CSE; 1%; 1 cigarette) for 24h. CSE induced the productions of IL-1β, TNF-α, IL-10, IL-4 and IFN-γ as well as the activations of NF-κB and STAT3 and the expression of ALX/FPR2 receptor. AT-RvD1 reduced the IL-1β and TNF-α production and increased the production of IFN-γ, while the production of IL-4 and IL-10 were not altered, in the cells stimulated by CSE when compared to CSE group. These effects were reversed BOC2, an antagonist of ALX/FPR2 receptor for AT-RvD1. In addition, AT-RvD1 reduced the phosphorylation of NF-κB and STAT3 when compared to CSE-stimulated BEAS-2B cells. No alteration of ALX/FPR2 expression was observed by AT-RvD1 when compared to CSE group. In the human monocytic leukemia cell line, the relative number of copies of IL-1β and IL-4 was significantly higher in CSE + AT-RvD1 group compared CSE group, however, the expression of M1 cytokine is more pronounced than M2 profile. AT-RvD1 could be an important target for the reduction of inflammation in the airways associated with smoking.