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.
【저자키워드】 SARS-CoV-2, COVID 19, immune responses, Cell-mediated immunity, mast cells (MC), interleukin-4 (IL-4), 【초록키워드】 COVID-19, pandemic, Pneumonia, Innate immunity, Transcription, lung, mast cell, Histopathology, Endothelial dysfunction, immunothrombosis, Spread, cells, edema, Control, membrane, plasma, upper airway, group, expression, patients, SARS-CoV-2 replication, IL-4, biopsy, Factor, specimen, positive, diffusion, alveolar injury, alveolar septa, Future, Prevent, Cell, interstitial, recruited, pneumocyte, upregulating, perivascular, alveolar lumen, MCs, post-mortem lung, septal, the cytokine storm, 【제목키워드】 COVID-19, septa,