Journal
FRONTIERS IN IMMUNOLOGY
Volume 11, Issue -, Pages -Publisher
FRONTIERS MEDIA SA
DOI: 10.3389/fimmu.2020.574862
Keywords
SARS-CoV-2; COVID 19; mast cells (MC); cell-mediated immunity; immune responses; interleukin-4 (IL-4)
Categories
Funding
- CAPES COVID 19 scholarship
- FAPERJ/Pronex [E-26/210.899/2016, CNE E-26/202.911/2017 CNPQ/Uni 432841/2016-4]
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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.
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