Abstract
This study involves the histological analysis of samples taken during autopsies in cases of COVID-19 related death to evaluate the inflammatory cytokine response and the tissue localization of the virus in various organs. In all the selected cases, SARS-CoV-2 RT-PCR on swabs collected from the upper (nasopharynx and oropharynx) and/or the lower respiratory (trachea and primary bronchi) tracts were positive. Tissue localization of SARS-CoV-2 was detected using antibodies against the nucleoprotein and the spike protein. Overall, we tested the hypothesis that the overexpression of proinflammatory cytokines plays an important role in the development of COVID-19-associated pneumonia by estimating the expression of multiple cytokines (IL-1β, IL-6, IL-10, IL-15, TNF-α, and MCP-1), inflammatory cells (CD4, CD8, CD20, and CD45), and fibrinogen. Immunohistochemical staining showed that endothelial cells expressed IL-1β in lung samples obtained from the COVID-19 group (p < 0.001). Similarly, alveolar capillary endothelial cells showed strong and diffuse immunoreactivity for IL-6 and IL-15 in the COVID-19 group (p < 0.001). TNF-α showed a higher immunoreactivity in the COVID-19 group than in the control group (p < 0.001). CD8 + T cells where more numerous in the lung samples obtained from the COVID-19 group (p < 0.001). Current evidence suggests that a cytokine storm is the major cause of acute respiratory distress syndrome (ARDS) and multiple organ failure and is consistently linked with fatal outcomes.
Highlights
On December 2019 the China Health Authority alerted the World Health Organization (WHO) about several cases of pneumonia with unknown etiology [1,2,3,4,5]
The aim of this study was to clarify the correlation between infection due to SARS-COV-2 and the inflammatory response, and to investigate the expression of cytokines such as tumor necrosis factor-α (TNF-α), IL-1β, IL-6, MCP-1, IL-10, IL-15, and leukocyte marker (CD 4, CD 8, CD20, CD 45), in an attempt to verify and define the role and expression of cytokines and mechanisms of cell death triggered in cases of COVID-19 deaths
Activated resident macrophages and pneumocytes initiate an inflammatory response triggered by the presence of SARS-CoV-2 in the lungs, leading to the overproduction of proinflammatory cytokines and chemokines, which are involved in endothelial cell apoptosis, increased vascular permeability, pulmonary exudation, hypoxia, and multiple organ failure [86]
Summary
On December 2019 the China Health Authority alerted the World Health Organization (WHO) about several cases of pneumonia with unknown etiology [1,2,3,4,5]. Laboratory diagnosis of a new disease, termed coronavirus disease 2019 (COVID-19), was performed using throat swab samples of 41 patients hospitalized on January 2, 2020 [6,7,8,9,10,11,12]. These authors contributed : Margherita Neri, Stefano D’Errico. The WHO classified the causal agent of COVID-19, called the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). The occurrence of infections between families supported the idea that
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