Anti-inflammatory actions of hyperoxia
Abstract
The mainstay treatment for decompression sickness (DCS) is recompression therapy with hyperbaric oxygen (HBO2). This practice was established based on a view that DCS is caused by inert gas bubbles and HBO2 can diminish bubble volume and hasten inert gas elimination. However, evidence now suggests that DCS is caused by inflammatory mediators due to oxidative stress initiated by elevations of gas partial pressure. Hence, the benefit of HBO2 for DCS is unexplained. We hypothesize that the benefit of HBO2 in DCS treatment is due to biochemical changes in neutrophils triggered by hyperoxia. Specifically, we hypothesize that protein S-nitrosylation of #-actin impairs inflammatory microparticle (MPs) production and assembly of the NLRP3 inflammasome, events that appear to establish a pro-inflammatory state in humans exposed to high pressure and cause systemic injuries in a murine model. This project will investigate the impact of HBO2 on human neutrophils, MPs and related immune responses. In Aim 1 studies will be performed using blood obtained from SCUBA divers who are undergoing HBO2 treatment for DCS. In Aim 2 we will discern basic anti-inflammatory mechanisms with studies of human cells exposed to HBO2 ex vivo.
Document Details
- Document Type
- DoD Grant Award
- Publication Date
- Nov 08, 2024
- Source ID
- N000142412549
Entities
People
- Stephen R. Thom
Organizations
- Office of Naval Research
- United States Navy
- University of Maryland