Abstract
BackgroundAcute 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.MethodsTo 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.ResultsMice 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).ConclusionsThe results suggest that hydrogen inhalation inhibits the deterioration of respiratory physiological function and alveolar fibrosis in this model of lung injury.
Highlights
Excessive, non-specific inflammation in the lungs initiates pathological processes leading to acute lung injury (ALI) and acute respiratory distress syndrome (ARDS), which directly and indirectly cause destruction of lungAokage et al BMC Pulm Med (2021) 21:339 tissue including alveolar structures [1]
Hydrogen inhalation for 21 days mitigates respiratory physiological dysfunction during fibrotic phase after bleomycin‐induced lung injury While Inspiratory capacity (IC) and Rs were not significantly different between mice that received hydrogen therapy and mice that received sham/air therapy (BH group vs. Bleomycin administration and air inhalation (BA) group, Fig. 1a, b) when we examine respiratory physiology, Static compliance (Cst), an index of the distensibility of the respiratory system, was significantly higher in mice that received hydrogen therapy (BH 0.056 mL/cm H2O [95% confidence interval (CI) 0.47–0.64] vs. BA 0.042 mL/cm H 2O [95% CI 0.031–0.053], p = 0.02) (Fig. 1c)
These results suggests that hydrogen inhalation therapy preserved the ability of the lung to expand and reduced lung stiffness
Summary
Non-specific inflammation in the lungs initiates pathological processes leading to acute lung injury (ALI) and acute respiratory distress syndrome (ARDS), which directly and indirectly cause destruction of lungAokage et al BMC Pulm Med (2021) 21:339 tissue including alveolar structures [1]. Non-specific inflammation in the lungs initiates pathological processes leading to acute lung injury (ALI) and acute respiratory distress syndrome (ARDS), which directly and indirectly cause destruction of lung. Seven to 10 days after onset, proliferation of type II alveolar epithelial cells and fibroblasts is observed in the destroyed alveoli (proliferative phase) [1]. This process of reconstruction is accompanied by persistent inflammation can promote alveolar fibrosis and decrease alveolar compliance (fibrotic phase). Acute respiratory distress syndrome, which is caused by acute lung injury, is a destructive respiratory disorder caused by a systemic inflammatory response. 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 inhibit lung fibrosis during late-phase lung injury
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
