| Autor: |
Vaz de Paula CB; School of Medicine, Postgraduate Program of Health Sciences, Pontifícia Universidade Católica do Paraná-PUCPR, Rua Imaculada Conceição, 1155 - Prado Velho, Curitiba, PR, Brazil. carolbvaz@gmail.com., de Azevedo MLV; Laboratory of Experimental Pathology, School of Medicine, Pontifícia Universidade Católica do Paraná-PUCPR, R. Imaculada Conceição, 1155 - Prado Velho, Curitiba, PR, Brazil., Nagashima S; School of Medicine, Postgraduate Program of Health Sciences, Pontifícia Universidade Católica do Paraná-PUCPR, Rua Imaculada Conceição, 1155 - Prado Velho, Curitiba, PR, Brazil., Martins APC; Laboratory of Experimental Pathology, School of Medicine, Pontifícia Universidade Católica do Paraná-PUCPR, R. Imaculada Conceição, 1155 - Prado Velho, Curitiba, PR, Brazil., Malaquias MAS; School of Medicine, Postgraduate Program of Health Sciences, Pontifícia Universidade Católica do Paraná-PUCPR, Rua Imaculada Conceição, 1155 - Prado Velho, Curitiba, PR, Brazil., Miggiolaro AFRDS; School of Medicine, Postgraduate Program of Health Sciences, Pontifícia Universidade Católica do Paraná-PUCPR, Rua Imaculada Conceição, 1155 - Prado Velho, Curitiba, PR, Brazil., da Silva Motta Júnior J; School of Medicine, Postgraduate Program of Health Sciences, Pontifícia Universidade Católica do Paraná-PUCPR, Rua Imaculada Conceição, 1155 - Prado Velho, Curitiba, PR, Brazil., Avelino G; Hospital Marcelino Champagnat, School of Medicine, Pontifical Catholic University of Paraná-PUCPR, R. Imaculada Conceição, 1155 - Prado Velho, Curitiba, PR, Brazil., do Carmo LAP; School of Medicine, Pontifícia Universidade Católica do Paraná-PUCPR, R. Imaculada Conceição, 1155 - Prado Velho, Curitiba, PR, Brazil., Carstens LB; School of Medicine, Pontifícia Universidade Católica do Paraná-PUCPR, R. Imaculada Conceição, 1155 - Prado Velho, Curitiba, PR, Brazil., de Noronha L; Laboratory of Experimental Pathology, School of Medicine, Pontifícia Universidade Católica do Paraná-PUCPR, R. Imaculada Conceição, 1155 - Prado Velho, Curitiba, PR, Brazil. |
| Abstrakt: |
The COVID-19 fatality rate is high when compared to the H1N1pdm09 (pandemic Influenza A virus H1N1 subtype) rate, and although both cause an aggravated inflammatory response, the differences in the mechanisms of both pandemic pneumonias need clarification. Thus, our goal was to analyze tissue expression of interleukins 4, 13, (IL-4, IL-13), transforming growth factor-beta (TGF-β), and the number of M2 macrophages (Sphingosine-1) in patients who died by COVID-19, comparing with cases of severe pneumopathy caused by H1N1pdm09, and a control group without lung injury. Six lung biopsy samples of patients who died of SARS-CoV-2 (COVID-19 group) were used and compared with ten lung samples of adults who died from a severe infection of H1N1pdm09 (H1N1 group) and eleven samples of patients who died from different causes without lung injury (CONTROL group). The expression of IL-4, IL-13, TGF-β, and M2 macrophages score (Sphingosine-1) were identified through immunohistochemistry (IHC). Significantly higher IL-4 tissue expression and Sphingosine-1 in M2 macrophages were observed in the COVID-19 group compared to both the H1N1 and the CONTROL groups. A different mechanism of diffuse alveolar damage (DAD) in SARS-CoV-2 compared to H1N1pdm09 infections were observed. IL-4 expression and lung remodeling are phenomena observed in both SARS-CoV-2 and H1N1pdm09. However, SARS-CoV-2 seems to promote lung damage through different mechanisms, such as the scarce participation Th1/Th17 response and the higher participation of the Th2. Understanding and managing the aggravated and ineffective immune response elicited by SARS-CoV-2 merits further clarification to improve treatments propose. |
