Hydrogen Gas Reduces Lung Damage and Improves Breathing in Mice

Authors
Journal
BMC Pulmonary Medicine
Year
DOI
10.1186/s12890-021-01712-2
Study Type
Mouse
Outcome
Positive
Peer Reviewed
Yes
Country
Japan
Health Condition
Acute Respiratory Distress Syndrome
Body System
Respiratory

TL;DR

Breathing in hydrogen gas daily may help reduce lung damage and scarring in mice with a lung injury similar to severe respiratory distress in humans.

Key Finding

Mice with bleomycin-induced lung injury that inhaled hydrogen gas daily for 21 days had significantly better lung function and less lung scarring than untreated mice, along with reduced inflammatory markers.

Summary

Researchers gave mice a lung injury using a drug called bleomycin, then exposed some mice to hydrogen gas (mixed with air) for 6 hours daily for 21 days, while others breathed regular air. Mice that inhaled hydrogen gas showed better lung function (their lungs were more flexible and easier to inflate) and less scarring compared to mice that only breathed air. The hydrogen treatment also reduced inflammatory markers (chemical signals that cause swelling and damage) in the lungs.

Practical Takeaway

This early-stage mouse study suggests hydrogen gas inhalation may help prevent lung scarring and preserve breathing function after severe lung injury. However, this is animal research only—human studies would be needed to determine if these benefits apply to people with acute lung injury or ARDS. The findings are promising but not yet applicable to clinical practice.

Abstract

Background: Acute respiratory distress syndrome, which is caused by acute lung injury, is a destructive respiratory disorder caused by a systemic inflammatory response. Persistent inflammation results in irreversible alveolar fibrosis. Because hydrogen gas possesses anti-inflammatory properties, we hypothesized that daily repeated inhalation of hydrogen gas could suppress persistent lung inflammation by inducing functional changes in macrophages, and consequently inhibit lung fibrosis during late-phase lung injury. Methods: To test this hypothesis, lung injury was induced in mice by intratracheal administration of bleomycin (1.0 mg/kg). Mice were exposed to control gas (air) or hydrogen (3.2% in air) for 6 h every day for 7 or 21 days. Respiratory physiology, tissue pathology, markers of inflammation, and macrophage phenotypes were examined. Results: Mice with bleomycin-induced lung injury that received daily hydrogen therapy for 21 days (BH group) exhibited higher static compliance (0.056 mL/cmH2O, 95% CI 0.047-0.064) than mice with bleomycin-induced lung injury exposed only to air (BA group; 0.042 mL/cmH2O, 95% CI 0.031-0.053, p = 0.02) and lower static elastance (BH 18.8 cmH2O/mL, [95% CI 15.4-22.2] vs. BA 26.7 cmH2O/mL [95% CI 19.6-33.8], p = 0.02). When the mRNA levels of pro-inflammatory cytokines were examined 7 days after bleomycin administration, interleukin (IL)-6, IL-4 and IL-13 were significantly lower in the BH group than in the BA group. There were significantly fewer M2-biased macrophages in the alveolar interstitium of the BH group than in the BA group (3.1% [95% CI 1.6-4.5%] vs. 1.1% [95% CI 0.3-1.8%], p = 0.008). Conclusions: The results suggest that hydrogen inhalation inhibits the deterioration of respiratory physiological function and alveolar fibrosis in this model of lung injury.