Ascorbic acid supplementation diminishes microparticle elevations and neutrophil activation following SCUBA diving

Yang, Ming; Barak, Otto; Dujić, Željko; Madden, Dennis; Bhopale, Veena M.; Bhullar, Jasjeet; Thom, Stephen R.

doi:10.1152/ajpregu.00155.2015

Cited by 15 publications

(17 citation statements)

References 31 publications

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“…There is evidence showing that the production of microparticles is elevated following diving. 3 15 16 Thom et al 16 found that microparticles could initiate decompression-induced neutrophil activation, and our group also showed bubbles could induce the production of microparticles in endothelial cells in vitro . 17 Whether microparticles may further induce the shift of macrophage phenotype will be validated in our future studies.…”

Section: Discussionsupporting

confidence: 53%

Polarization of macrophages in the blood after decompression in mice

Han

Zhang²,

Xu³

et al. 2017

Med Gas Res

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The veins are a major site of bubble formation after decompression and the lung is a target organ of bubbles. Bubble-induced inflammation has been implicated in the pathogenesis of decompression sickness (DCS). Macrophages play a central role in the inflammation, and macrophage polarization is closely related to the pathogenesis of some lung diseases. This study aimed to investigate the blood macrophage polarization in mice after decompression. BALB/c mice were exposed to hyperbaric air for 60 minutes, and rapid decompression was performed to induce DCS. Slow decompression and hyperoxia (150 kPa, 60 minutes) served as control groups, and hyperbaric oxygen (HBO; 250 kPa, 60 minutes) was employed for DCS treatment. Macrophage phenotype was determined by flow cytometry, and cytokines related to macrophage polarization were measured by enzyme-linked immunosorbent assay. Our results showed rapid decompression significantly induced the shift to M1 phenotype, which was not observed in slow decompression group, HBO and hyperoxia groups. These changes were consistent with the change in blood tumor necrosis factor α level. Moreover, any treatment could significantly increase the M2 macrophages, but blood interleukin-10 remained unchanged after different treatments. In addition, the blood and lung levels of monocyte chemoattractant protein-1 and intercellular adhesion molecule-1 increased significantly after rapid decompression, but reduced markedly after HBO treatment. Taken together, rapid decompression is able to induce the shift to M1 phenotype in blood macrophages, which may then migrate into the lung involving decompression-induced lung injury.

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Section: Discussionsupporting

confidence: 53%

Polarization of macrophages in the blood after decompression in mice

Han

Zhang²,

Xu³

et al. 2017

Med Gas Res

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“…Unlike after SCUBA diving, when two-to threefold increases were reported (Thom et al 2013), deep breath-hold dives with short surface times lead to a 65% increase, whereas long-lasting repetitive breath-hold dives lead to a 50% increase. Yang argued that besides hyperoxia (present in both SCUBA and BHD), high-pressure inert or ballast gas exposure is also crucial to increase MP levels (Yang et al 2015). In BHD, the only inert gas added is nitrogen that remained in the lungs.…”

Section: Discussionmentioning

confidence: 99%

Vascular dysfunction following breath-hold diving

Barak

Janjic

Drviš

et al. 2020

Can. J. Physiol. Pharmacol.

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The pathogenesis of predominantly neurological decompression sickness (DCS) is multifactorial. In SCUBA diving, besides gas bubbles, DCS has been linked to microparticle release, impaired endothelial function, and platelet activation. This study focused on vascular damage and its potential role in the genesis of DCS in breath-hold diving. Eleven breath-hold divers participated in a field study comprising eight deep breath-hold dives with short surface periods and repetitive breath-hold dives lasting for 6 h. Endothelium-dependent vasodilation of the brachial artery, via flow-mediated dilation (FMD), and the number of microparticles (MPs) were assessed before and after each protocol. All measures were analyzed by two-way within-subject ANOVA (2 × 2 ANOVA; factors: time and protocol). Absolute FMD was reduced following both diving protocols (p < 0.001), with no interaction (p = 0.288) or main effect of protocol (p = 0.151). There was a significant difference in the total number of circulating MPs between protocols (p = 0.007), where both increased post-dive (p = 0.012). The number of CD31+/CD41– and CD66b+ MP subtypes, although different between protocols (p < 0.001), also increased by 41.0% ± 56.6% (p = 0.050) and 60.0% ± 53.2% (p = 0.045) following deep and repetitive breath-hold dives, respectively. Both deep and repetitive breath-hold diving lead to endothelial dysfunction that may play an important role in the genesis of neurological DCS.

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“…The roles of MPs in chronic respiratory disorders also require study as they may contribute to risks for central nervous system, cardiovascular, and inflammatory bowel diseases (4, 10, 19). Further evaluations may also identify prophylactic interventions, as some relatively benign agents can abrogate MPs production in response to some stimuli (43) and dietary changes can inhibit the NLRP3 inflammasome (45).…”

Section: Discussionmentioning

confidence: 99%

Inflammatory responses to acute elevations of carbon dioxide in mice

Thom

Bhopale

et al. 2017

Journal of Applied Physiology

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Health risks are described from elevated indoor air carbon dioxide (CO), which often ranges from 1,000 to 4,000 ppm, but the mechanisms are unknown. Here, we demonstrate that mice exposed for 2 h to 2,000 or 4,000 ppm CO exhibit, respectively, 3.4 ± 0.9-fold (SE, = 6) and 4.1 ± 0.7-fold ( = 10) elevations in circulating microparticles (MPs); neutrophil and platelet activation, and vascular leak in brain, muscle, and distal colon. Interleukin (IL)-1β content of MPs also increases after 2,000 ppm by 3.8 ± 0.6-fold ( = 6) and after 4,000 ppm CO by 9.3 ± 1.1-fold ( = 10) greater than control. CO-induced vascular damage is abrogated by treating mice with an antibody to IL-1β or an IL-1β receptor inhibitor. Injecting naïve mice with CO-induced MPs expressing a protein found on mature neutrophils recapitulates vascular damage as seen with elevated CO, and destruction of MPs in CO-exposed mice abrogates vascular injuries without altering neutrophil or platelet activation. We conclude that environmentally relevant elevations of CO trigger neutrophils to generate MPs containing high concentrations of IL-1β that cause diffuse inflammatory vascular injury. Elevated levels of CO are often found in indoor air and cause adverse health effects, but the mechanisms have not been identified. In a murine model, environmentally relevant levels of CO were found to cause diffuse vascular damage because neutrophils are stimulated to produce microparticles that contain high concentrations of interleukin-1β.

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Ascorbic acid supplementation diminishes microparticle elevations and neutrophil activation following SCUBA diving

Cited by 15 publications

References 31 publications

Polarization of macrophages in the blood after decompression in mice

Polarization of macrophages in the blood after decompression in mice

Vascular dysfunction following breath-hold diving

Inflammatory responses to acute elevations of carbon dioxide in mice

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