Microparticle and interleukin-1β production with human simulated compressed air diving

Abstract

Production of blood-borne microparticles (MPs), 0.1–1 µm diameter vesicles, and interleukin (IL)-1β in response to high pressure is reported in lab animals and associated with pathological changes. It is unknown whether the responses occur in humans, and whether they are due to exposure to high pressure or to the process of decompression. Blood from research subjects exposed in hyperbaric chambers to air pressure equal to 18 meters of sea water (msw) for 60 minutes or 30 msw for 35 minutes were obtained prior to and during compression and 2 hours post-decompression. MPs and intra-particle IL-1β elevations occurred while at pressure in both groups. At 18 msw (n = 15) MPs increased by 1.8-fold, and IL-1β by 7.0-fold (p < 0.05, repeated measures ANOVA on ranks). At 30 msw (n = 16) MPs increased by 2.5-fold, and IL-1β by 4.6-fold (p < 0.05), and elevations persisted after decompression with MPs elevated by 2.0-fold, and IL-1β by 6.0-fold (p < 0.05). Whereas neutrophils incubated in ambient air pressure for up to 3 hours ex vivo did not generate MPs, those exposed to air pressure at 180 kPa for 1 hour generated 1.4 ± 0.1 MPs/cell (n = 8, p < 0.05 versus ambient air), and 1.7 ± 0.1 MPs/cell (p < 0.05 versus ambient air) when exposed to 300 kPa for 35 minutes. At both pressures IL-1β concentration tripled (p < 0.05 versus ambient air) during pressure exposure and increased 6-fold (p < 0.05 versus ambient air) over 2 hours post-decompression. Platelets also generated MPs but at a rate about 1/100 that seen with neutrophils. We conclude that production of MPs containing elevated concentrations of IL-1β occur in humans during exposure to high gas pressures, more so than as a response to decompression. While these events may pose adverse health threats, their contribution to decompression sickness development requires further study.

Elevations of Extracellular Vesicles and Inflammatory Biomarkers in Closed Circuit SCUBA Divers

“…However, the inconsistent presence of bubbles in human studies has prompted investigations that are focused instead on inflammatory pathways [ 1 , 2 , 3 ]. A body of work implicates a subset of extracellular vesicles (EVs), 0.1 to 1 µm microparticles (MPs), that are elevated in humans and rodent models exposed to high gas pressure and rise further after decompression [ 4 , 5 , 6 , 7 , 8 , 9 , 10 , 11 , 12 , 13 , 14 , 15 ]. MPs initiate a systemic inflammatory response related to neutrophil activation [ 13 , 16 , 17 , 18 ].…”

Varying Oxygen Partial Pressure Elicits Blood-Borne Microparticles Expressing Different Cell-Specific Proteins—Toward a Targeted Use of Oxygen?

“…The literature has identified several contributing factors to pressure exposures and DCS, such as vascular dysfunction, oxidative stress, and blood-borne microparticles (MPs) [ 26 , 27 ], which have been considered potential targets for pre-conditioning interventions. MPs are of particular interest since a growing body of data suggest that they are a potential bubble nucleation site and play a role in DCS pathophysiology [ 27 , 28 , 29 , 30 , 31 ]. MPs are 0.1–1 µm vesicles generated by an outward budding of the plasma membrane in a process that results in the surface expression of phosphatidylserine.…”

“…It is known to occur with diving and documented as the upregulation of antioxidant genes and elevation of plasma and intracellular antioxidant enzyme levels [ 37 , 38 , 39 , 40 , 41 , 42 ]. High-pressure exposures also increase the number of MPs in human divers, marine mammals, and small animals used in models of DCS [ 27 , 28 , 29 , 30 , 43 , 44 , 45 , 46 , 47 ]. Studies with isolated human and murine neutrophils demonstrate that MP production is an oxidative stress response [ 48 ].…”

Analysis of the Increase of Vascular Cell Adhesion Molecule-1 (VCAM-1) Expression and the Effect of Exposure in a Hyperbaric Chamber on VCAM-1 in Human Blood Serum: A Cross-Sectional Study

“…Exactly these results could be expected, because VCAM-1 is a key cell adhesion molecule involved in inflammation that is closely implicated in various immunological disorders [24,25]. The VCAM-1 protein mediates the adhesion of neutrophils, monocytes, eosinophils and basophils to the vascular endothelium [14,26]. It is also active in the signal transduction of leukocytes and endothelial cells [24,[27][28][29].…”