Author: Miggiolaro, Anna Flavia Ribeiro dos Santos; Motta Junior, Jarbas da Silva; de Paula, Caroline Busatta Vaz; Nagashima, Seigo; Malaquias, Mineia Alessandra Scaranello; Carstens, Lucas Baena; Novais, Andrea Moreno; Baena, Cristina Pellegrino; de Noronha, Lucia
Title: Covid-19 cytokine storm in pulmonary tissue: anatomopathological and immunohistochemical findings Cord-id: reuqypc0 Document date: 2020_11_12
ID: reuqypc0
Snippet: The COVID-19 pandemic is a worldwide threat, and information on physiopathological aspects of the disease is limited. Despite efforts in searching treatment options, a better understanding of the SARS-CoV-2 pathways can contribute to managing severe cases. In this study, we aim to describe pathological and immunopathogenic findings of two different cases, both in the high-risk group. Post-mortem lung biopsies were analyzed by traditional and immunohistochemical methods. Tissue expression of inna
Document: The COVID-19 pandemic is a worldwide threat, and information on physiopathological aspects of the disease is limited. Despite efforts in searching treatment options, a better understanding of the SARS-CoV-2 pathways can contribute to managing severe cases. In this study, we aim to describe pathological and immunopathogenic findings of two different cases, both in the high-risk group. Post-mortem lung biopsies were analyzed by traditional and immunohistochemical methods. Tissue expression of innate and adaptive immune response biomarkers was tested. We observed a higher innate response in case 1 with an abundance of mast cells, scarce CD8+ lymphocytes, high expression of TNF-alpha, and almost absent adaptative immune response. In case 2, the adaptative immune response was present, with numerous CD8+ lymphocytes and higher levels of IL-4 and TGF-beta. Both cases converged to a prothrombotic state expressing high IL-6, followed by ICAM-1 expression and endotheliites leading to systemic inflammatory response syndrome. In conclusion, differences in age and comorbidities and immune response described here may be related to the SARS-CoV-2 delay in the adaptative immune response, evolution stage of diffuse alveolar damage, and progression for systemic inflammatory response syndrome.
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