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Dissolved gases from pressure changes in the lungs elicit an immune response in human peripheral blood.

Authors
  • Harrell, Abigail G1
  • Thom, Stephen R2
  • Shields, C Wyatt 4th1, 3
  • 1 Department of Chemical and Biological Engineering, University of Colorado Boulder, Boulder, CO 80303, United States. , (United States)
  • 2 Department of Emergency Medicine, University of Maryland School of Medicine, Baltimore, MD 21201, United States. , (United States)
  • 3 Biomedical Engineering Program, University of Colorado Boulder, Boulder CO 80303, United States. , (United States)
Type
Published Article
Journal
bioRxiv : the preprint server for biology
Publication Date
Oct 21, 2023
Identifiers
DOI: 10.1101/2023.10.18.562856
PMID: 37904988
Source
Medline
Keywords
Language
English
License
Unknown

Abstract

Conventional dogma suggests that decompression sickness (DCS) is caused by nitrogen bubble nucleation in the blood vessels and/or tissues; however, the abundance of bubbles does not correlate with DCS severity. Since immune cells respond to chemical and environmental cues, we hypothesized that the elevated partial pressures of dissolved gases drive aberrant immune cell phenotypes in the alveolar vasculature. To test this hypothesis, we measured immune responses within human lung-on-a-chip devices established with primary alveolar cells and microvascular cells. Devices were pressurized to 1.0 or 3.5 atm and surrounded by normal alveolar air or oxygen-reduced air. Phenotyping of neutrophils, monocytes, and dendritic cells as well as multiplexed ELISA revealed that immune responses occur within 1 hour and that normal alveolar air (i.e., hyperbaric oxygen and nitrogen) confer greater immune activation. This work strongly suggests innate immune cell reactions initiated at elevated partial pressures contribute to the etiology of DCS.

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