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Covid-19 cytokine storm in pulmonary tissue: Anatomopathological and immunohistochemical findings

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 pathologi...

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Detalles Bibliográficos
Autores principales: Ribeiro dos Santos Miggiolaro, Anna Flavia, da Silva Motta Junior, Jarbas, Busatta Vaz de Paula, Caroline, Nagashima, Seigo, Alessandra Scaranello Malaquias, Mineia, Baena Carstens, Lucas, N Moreno-Amaral, Andrea, Pellegrino Baena, Cristina, de Noronha, Lucia
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Elsevier 2020
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7658564/
https://www.ncbi.nlm.nih.gov/pubmed/33200067
http://dx.doi.org/10.1016/j.rmcr.2020.101292
Descripción
Sumario: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.