Mast Cells in Alveolar Septa of COVID-19 Patients: A Pathogenic Pathway That May Link Interstitial Edema to Immunothrombosis.
Autor: | Motta Junior JDS; School of Medicine, Pontifícia Universidade Católica do Paraná PUCPR, Curitiba, Brazil.; Hospital Marcelino Champagnat, Curitiba, Brazil., Miggiolaro AFRDS; School of Medicine, Pontifícia Universidade Católica do Paraná PUCPR, Curitiba, Brazil.; Hospital Marcelino Champagnat, Curitiba, Brazil., Nagashima S; School of Medicine, Pontifícia Universidade Católica do Paraná PUCPR, Curitiba, Brazil., de Paula CBV; School of Medicine, Pontifícia Universidade Católica do Paraná PUCPR, Curitiba, Brazil., Baena CP; School of Medicine, Pontifícia Universidade Católica do Paraná PUCPR, Curitiba, Brazil.; Hospital Marcelino Champagnat, Curitiba, Brazil., Scharfstein J; Instituto de Biofísica Carlos Chagas Filho, Universidade Federal Do Rio de Janeiro, Rio de Janeiro, Brazil., de Noronha L; School of Medicine, Pontifícia Universidade Católica do Paraná PUCPR, Curitiba, Brazil. |
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Jazyk: | angličtina |
Zdroj: | Frontiers in immunology [Front Immunol] 2020 Sep 18; Vol. 11, pp. 574862. Date of Electronic Publication: 2020 Sep 18 (Print Publication: 2020). |
DOI: | 10.3389/fimmu.2020.574862 |
Abstrakt: | It is currently believed that innate immunity is unable to prevent the spread of SARS-CoV-2 from the upper airways to the alveoli of high-risk groups of patients. SARS-CoV-2 replication in ACE-2-expressing pneumocytes can drive the diffuse alveolar injury through the cytokine storm and immunothrombosis by upregulating the transcription of chemokine/cytokines, unlike several other respiratory viruses. Here we report histopathology data obtained in post-mortem lung biopsies of COVID-19, showing the increased density of perivascular and septal mast cells (MCs) and IL-4-expressing cells ( n = 6), in contrast to the numbers found in pandemic H1N1-induced pneumonia ( n = 10) or Control specimens ( n = 10). Noteworthy, COVID-19 lung biopsies showed a higher density of CD117 + cells, suggesting that c-kit positive MCs progenitors were recruited earlier to the alveolar septa. These findings suggest that MC proliferation/differentiation in the alveolar septa might be harnessed by the shift toward IL-4 expression in the inflamed alveolar septa. Future studies may clarify whether the fibrin-dependent generation of the hyaline membrane, processes that require the diffusion of procoagulative plasma factors into the alveolar lumen and the endothelial dysfunction, are preceded by MC-driven formation of interstitial edema in the alveolar septa. (Copyright © 2020 Motta Junior, Miggiolaro, Nagashima, de Paula, Baena, Scharfstein and de Noronha.) |
Databáze: | MEDLINE |
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