CHEST Guidelines-IL-33-Depletion-in-COVID-19-Lungs_2021

IL-33-Depletion-in-COVID-19-Lungs_2021_chest

Pdf Summary

This study investigates IL-33 expression in the lungs of COVID-19 patients, contrasting it with other inflammatory lung diseases such as chronic obstructive pulmonary disease (COPD) and idiopathic pulmonary fibrosis (IPF). IL-33, a key molecule involved in lung homeostasis and repair, is elevated in COPD and IPF but is nearly depleted in COVID-19 lung tissues. The analysis involved comparing de-identified postmortem lung samples from COVID-19 patients with controls and patients with other lung diseases.<br /><br />In COVID-19 cases, IL-33 expression was notably low, which is contrary to the elevated levels observed in other lung conditions. This depletion might suggest a significant lung-specific reduction of IL-33, potentially affecting the lung’s ability to repair and regenerate following infectious damage. COVID-19 samples also demonstrated minimal prosurfactant protein C-positive type II alveolar epithelial cells (AEC2), indicating possible cell death and diminished lung repair capabilities.<br /><br />The study was carried out by inspecting lung tissues for the presence of IL-33, vimentin (to assess mesenchymal cell presence), and pro-surfactant protein C using fluorescence microscopy. The findings indicated that while IL-33 was mostly nuclear and localized in endothelial and progenitor cells in control and diseased subjects, it was nearly absent in COVID-19 samples.<br /><br />These results highlight the contrast in cytokine behavior between COVID-19 and other chronic lung conditions, suggesting IL-33's nuanced role in respiratory diseases. Further investigation is suggested to assess if replenishment of IL-33 could be beneficial or detrimental in infections like COVID-19. The nuanced depletion indicates that more research is needed to understand IL-33's role and its potential as a therapeutic target for recovery in COVID-19 and similar diseases.

Keywords

IL-33 expression

COVID-19

inflammatory lung diseases

chronic obstructive pulmonary disease

idiopathic pulmonary fibrosis

lung homeostasis

postmortem lung samples

type II alveolar epithelial cells

fluorescence microscopy

cytokine behavior