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10.1016/j.rmcr.2020.101292

http://scihub22266oqcxt.onion/10.1016/j.rmcr.2020.101292
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suck abstract from ncbi


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pmid33200067      Respir+Med+Case+Rep 2020 ; 31 (ä): 101292
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  • Covid-19 cytokine storm in pulmonary tissue: Anatomopathological and immunohistochemical findings #MMPMID33200067
  • Ribeiro Dos Santos Miggiolaro AF; da Silva Motta Junior J; Busatta Vaz de Paula C; Nagashima S; Alessandra Scaranello Malaquias M; Baena Carstens L; N Moreno-Amaral A; Pellegrino Baena C; de Noronha L
  • Respir Med Case Rep 2020[]; 31 (ä): 101292 PMID33200067show ga
  • 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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