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The des-Arg9-bradykinin/B1R axis: Hepatic damage in COVID-19

2022; Frontiers Media; Volume: 13; Linguagem: Inglês

10.3389/fphys.2022.1080837

1664-042X

Gabriel Moreira de Mello Mendes, Israel Júnior Borges do Nascimento, Paulo HS. Marazzi-Diniz, Izabela Boueri da Silveira, Matheus F. Itaborahy, Luiz E. Viana, Filipe Alex da Silva, Monique Freire Santana, Rebecca AA. Pinto, Bruna Guimarães Dutra, Marcus Lacerda, Stanley A. Araujo, David Campos Wanderley, Paula Vieira Teixeira Vidigal, Paulo HC Diniz, Thiago Verano‐Braga, Robson A.S. Santos, M. Fátima Leite,

Coagulation, Bradykinin, Polyphosphates, and Angioedema

Patients infected by the SARS-CoV-2 virus are commonly diagnosed with threatening liver conditions associated with drug-induced therapies and systemic viral action. RNA-Seq data from cells in bronchoalveolar lavage fluid from COVID-19 patients have pointed out dysregulation of kallikrein-kinin and renin-angiotensin systems as a possible mechanism that triggers multi-organ damage away from the leading site of virus infection. Therefore, we measured the plasma concentration of biologically active peptides from the kallikrein-kinin system, bradykinin and des-Arg 9 -bradykinin, and liver expression of its proinflammatory axis, bradykinin 1 receptor (B1R). We measured the plasma concentration of bradykinin and des-Arg 9 -bradykinin of 20 virologically confirmed COVID-19 patients using a liquid chromatography-tandem mass spectrometry-based methodology. The expression of B1R was evaluated by immunohistochemistry from post-mortem liver specimens of 27 COVID-19 individuals. We found a significantly higher blood level of des-Arg 9 -bradykinin and a lower bradykinin concentration in patients with COVID-19 compared to a healthy, uninfected control group. We also observed increased B1R expression levels in hepatic tissues of patients with COVID-19 under all hepatic injuries analyzed (liver congestion, portal vein dilation, steatosis, and ischemic necrosis). Our data indicate that des-Arg 9 -bradykinin/B1R is associated with the acute hepatic dysfunction induced by the SARS-CoV-2 virus infection in the pathogenesis of COVID-19.