IL-33 Depletion in COVID-19 Lungs

Details

• Personal Author:
  Anderson DR ; Bailey KL ; Dickinson JD ; Duryee MJ ; England BR ; Gaurav R ; Katafiasz DM ; Mikuls TR ; Nelson AJ ; Poole JA ; Radio SJ ; Romberger DJ ; Strah HM ; Thiele GM ; Wyatt TA
• Description:
  IL-33 is an alarmin that plays an integral role in lung homeostasis through its actions in wound repair, fibrosis, and remodeling processes. Stored in the nucleus, IL-33 is released to the cytoplasm and extracellular fluids following insult or damage that was induced by various infectious, noxious, or environmental agents. In addition to its role in allergic asthma, studies have demonstrated elevated IL-33 in COPD plasma, COPD airways, and idiopathic pulmonary fibrosis (IPF) lung tissues; however, a comparative analysis of lung IL-33 expression in the setting of infectious sequalae are lacking. Infection with SARS-CoV-2 causes an inflammatory cascade that results in reduced diffusion capacity, hypoxia, and death. The Rapid Evidence Appraisal for COVID-19 Therapies (REACT) COVID investigators screened serum from 100 subjects with COVID-19 for cytokines (ie, IL-6, tumor necrosis factor, IL-8, IL-1beta, granulocyte-macrophage colony-stimulating factor, IL-33, interferon-gamma, IL-10) and found that increased serum IL-33 levels (as well as tumor necrosis factor) were independently predictive of poor outcomes with SARS-CoV-2 in patients <70 years old (adjusted OR for IL-33, 11.14; 95% CI, 1.01-123.72). The objective of this study was to characterize IL-33 expression in the lungs of patients with fulminant COVID-19, comparing this expression with that observed in other inflammatory lung diseases. ... In conclusion, these studies strengthen the relationship of IL-33 in COVID-19 to suggest that additional and longitudinal assessments are warranted to understand the mechanisms and timing of lung IL-33 expression and regulation for promoting damage or driving wound repair processes to inform potential interventional strategies. [Description provided by NIOSH]
• Subjects:
  Communicable Diseases Genetics Immune System Lung Occupational Health Respiratory System Safety
• Keywords:
  COVID-19 Cytokines Genes Immune Reaction Lung Cells Lung Function Proteins SARS-CoV-2
• ISSN:
  0012-3692
• Document Type:
  Text
• Funding:
  Cooperative Agreement
• Genre:
  Journal Article
• Place as Subject:
  Nebraska ; OSHA Region 7
• CIO:
  National Institute for Occupational Safety and Health (NIOSH)
• Topic:
  Workplace Safety & Health
• Location:
  North America
• Volume:
  160
• Issue:
  5
• NIOSHTIC Number:
  nn:20064031
• Citation:
  Chest 2021 Nov; 160(5):1656-1659
• Contact Point Address:
  Jill A. Poole, MD, Division of Allergy & Immunology, Department of Internal Medicine,University of Nebraska Medical Center, Omaha, NE
• Email:
  japoole@unmc.edu
• Federal Fiscal Year:
  2022
• NORA Priority Area:
  Agriculture, Forestry and Fishing
• Performing Organization:
  University of Nebraska Medical Center - Omaha
• Peer Reviewed:
  False
• Start Date:
  20110901
• Source Full Name:
  Chest
• End Date:
  20270831
• Collection(s):
  National Institute for Occupational Safety and Health
• Main Document Checksum:
  urn:sha-512:48129a374c7c3a6f5f45cb1a862580ee73cebbd9c2a36bf9a93fe3072ad743b133b4e52eb49a891f2b2f399d5b4fd392cc8bfe37c0cde92316ccb3e7fc01fccc
• Download URL:
  https://stacks.cdc.gov/view/cdc/222558/cdc_222558_DS1.pdf
• File Type:
  [PDF - 1.70 MB ]