Relevance of angiotensin-(1-7) and its receptor Mas in pneumonia caused by influenza virus and post-influenza pneumococcal infection

dc.creatorMelo, Eliza Mathias
dc.creatorSarto, Juliana Del
dc.creatorVago, Juliana Priscila
dc.creatorTavares, Luciana Pádua
dc.creatorRago, Flávia
dc.creatorGonçalves, Ana Paula F
dc.creatorMachado, Marina Gomes
dc.creatorAranda-Pardos, Irene
dc.creatorValiate, Bruno Vinícius Santos
dc.creatorCassali, Geovanni Dantas
dc.creatorPinho, Vanessa
dc.creatorSousa, Lirlândia Pires de
dc.creatorA-Gonzalez, Noelia
dc.creatorSantos, Maria José Campagnole
dc.creatorBader, Michael
dc.creatorSantos, Robson Augusto Souza dos
dc.creatorMachado, Alexandre de Magalhães Vieira
dc.creatorLudwig, Stephan
dc.creatorTeixeira, Mauro Martins
dc.date2022-02-17T18:20:02Z
dc.date2022-02-17T18:20:02Z
dc.date2021
dc.date.accessioned2023-09-27T00:12:54Z
dc.date.available2023-09-27T00:12:54Z
dc.identifierMELO, Eliza Mathias et al. Relevance of angiotensin-(1-7) and its receptor Mas in pneumonia caused by influenza virus and post-influenza pneumococcal infection. Pharmacol Res., v. 163, 105292, 2021 doi: 10.1016/j.phrs.2020.105292.
dc.identifier1043-6618
dc.identifierhttps://www.arca.fiocruz.br/handle/icict/51275
dc.identifier.urihttps://repositorioslatinoamericanos.uchile.cl/handle/2250/8898590
dc.descriptionResolution failure of exacerbated inflammation triggered by Influenza A virus (IAV) prevents return of pulmonary homeostasis and survival, especially when associated with secondary pneumococcal infection. Therapeutic strategies based on pro-resolving molecules have great potential against acute inflammatory diseases. Angiotensin-(1-7) [Ang-(1-7)] is a pro-resolving mediator that acts on its Mas receptor (MasR) to promote resolution of inflammation. We investigated the effects of Ang-(1-7) and the role of MasR in the context of primary IAV infection and secondary pneumococcal infection and evaluated pulmonary inflammation, virus titers and bacteria counts, and pulmonary damage. Therapeutic treatment with Ang-(1-7) decreased neutrophil recruitment, lung injury, viral load and morbidity after a primary IAV infection. Ang-(1-7) induced apoptosis of neutrophils and efferocytosis of these cells by alveolar macrophages, but had no direct effect on IAV replication in vitro. MasR-deficient (MasR-/-) mice were highly susceptible to IAV infection, displaying uncontrolled inflammation, increased viral load and greater lethality rate, as compared to WT animals. Ang-(1-7) was not protective in MasR-/- mice. Interestingly, Ang-(1-7) given during a sublethal dose of IAV infection greatly reduced morbidity associated with a subsequent S. pneumoniae infection, as seen by decrease in the magnitude of neutrophil influx, number of bacteria in the blood leading to a lower lethality. Altogether, these results show that Ang-(1-7) is highly protective against severe primary IAV infection and protects against secondary bacterial infection of the lung. These effects are MasR-dependent. Mediators of resolution of inflammation, such as Ang-(1-7), should be considered for the treatment of pulmonary viral infections.
dc.formatapplication/pdf
dc.languageeng
dc.publisherElsevier
dc.rightsrestricted access
dc.subjectAngiotensin-(1-7)
dc.subjectInfection
dc.subjectInflammation
dc.subjectInfluenza virus
dc.subjectResolution
dc.subjectStreptococcus pneumoniae
dc.titleRelevance of angiotensin-(1-7) and its receptor Mas in pneumonia caused by influenza virus and post-influenza pneumococcal infection
dc.typeArticle


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