分子状水素はIL-33/ILC2軸の抑制を介して喘息を緩和する
Using an OVA-sensitized asthmatic mouse model and a house dust mite (HDM)-stimulated 16HBE bronchial epithelial cell model, this study examined the effects of hydrogen/oxygen gas mixture on type II airway inflammation. In OVA-challenged mice, serum and bronchoalveolar lavage fluid concentrations of IL-33 and other type II cytokines were markedly elevated; hydrogen administration significantly reduced these levels. NF-κB (p65) and ST2 expression were upregulated by OVA and downregulated by hydrogen. The ILC2 population expanded in asthmatic mice was substantially reduced following hydrogen exposure. Airway epithelial junction proteins E-cadherin and ZO-1, diminished in asthmatic mice, were restored by hydrogen. In HDM-treated 16HBE cells, hydrogen attenuated apoptosis, suppressed IL-33 and ST2 upregulation, and reduced IL-33 promoter activity as measured by dual-luciferase assay. miRNA array profiling identified a distinct set of differentially expressed miRNAs in HDM-exposed cells that were modulated by hydrogen co-treatment. Collectively, these findings indicate that molecular hydrogen suppresses allergen-driven type II inflammation through the IL-33/ILC2 axis.
Molecular hydrogen suppresses NF-κB (p65) activation, thereby reducing IL-33 promoter activity and ST2 expression, which in turn limits ILC2 expansion and downstream type II inflammatory cytokine production.
For inhalation applications of molecular hydrogen, the lower flammability limit (LFL) deserves careful handling. The classical 4% figure applies to closed-system mixtures; the practical inhalation-environment threshold is 10%. Even pure-hydrogen output (the UFL 75% paradox) passes through the flammable range at the air–gas boundary. High-concentration (66% / 100%) inhalers are documented in the Japanese Consumer Affairs Agency accident-information database and are not recommended.
See also:
https://h2-papers.org/en/papers/33852061