# Hydrogen inhalation ameliorates lung inflammation in mice with asthma

**Authors:** Hongchang Li, Xia Qi, Hongyan Xu, Rong Zhou, Xiaochun Liu, Lei Li, Cuiping Hu, Chunli Dai

PMC · DOI: 10.1186/s40001-025-03296-7 · European Journal of Medical Research · 2025-10-27

## TL;DR

Inhaling hydrogen gas reduces lung inflammation in mice with asthma, suggesting it could be a promising treatment.

## Contribution

This study demonstrates hydrogen inhalation as a novel therapeutic approach for asthma by reducing inflammation and immune response.

## Key findings

- Hydrogen inhalation reduced airway hyperreactivity and inflammation in asthmatic mice.
- Hydrogen treatment increased anti-inflammatory cytokines IL-10 and TGF-β1 while decreasing IL-4, IL-5, and IL-13.
- Hydrogen reduced pathological damage in lung tissues and oxidative stress markers like MDA while increasing SOD.

## Abstract

Asthma, a prevalent noninfectious chronic disease characterized by type II inflammation, features airway hyperreactivity, bronchoconstriction, and airway remodeling, ultimately causing widespread airway narrowing. Hydrogen has been shown to exhibit antioxidant and anti-inflammatory properties that are beneficial for a range of diseases. This study initially investigated the ameliorative effects of hydrogen gas inhalation on lung inflammation in mice with asthma induced by ovalbumin (OVA). The mice were first sensitized with OVA and subsequently exposed to nebulized 1% OVA via the airway to induce an asthma model. Hydrogen was inhaled for 7 consecutive days as a therapeutic intervention to detect changes in various indicators. Compared with the control treatment, hydrogen inhalation significantly mitigated OVA-induced airway hyperreactivity and inflammation. Hydrogen inhalation attenuated the immune response; decreased the levels of IL-4, IL-5 and IL-13; and further increased the mRNA expression levels of Treg-associated cytokines, namely, IL-10 and TGF-β1, thereby bolstering the body's inflammatory resistance mechanisms. In addition, it also reduced total serum IgE levels and malondialdehyde (MDA) production and increased superoxide dismutase (SOD) secretion in lung tissue. The histological analysis of lung tissues revealed that OVA induced prominent inflammatory cell infiltration and cell proliferation in the alveolar wall, which were markedly ameliorated in the hydrogen-treated group, indicating reduced pathological damage. These findings indicate that hydrogen inhalation effectively suppresses OVA-induced asthma, leading to a substantial improvement in associated lung inflammation, and that the inhalation of hydrogen may be a more feasible approach for future asthma treatment strategies.

## Linked entities

- **Proteins:** IL4 (interleukin 4), IL5 (interleukin 5), IL13 (interleukin 13), IL10 (interleukin 10), TGFB1 (transforming growth factor beta 1), SOD1 (superoxide dismutase 1), so (sine oculis)
- **Chemicals:** hydrogen (PubChem CID 783), IgE (PubChem CID 19920)
- **Diseases:** asthma (MONDO:0004979)
- **Species:** Mus musculus (taxon 10090)

## Full-text entities

- **Genes:** Il13 (interleukin 13) [NCBI Gene 16163] {aka Il-13}, Serpinb1-ps1 (serine (or cysteine) peptidase inhibitor, clade B, member 1, pseudogene) [NCBI Gene 282665] {aka EID, ovalbumin}, Tgfb1 (transforming growth factor, beta 1) [NCBI Gene 21803] {aka TGF-beta1, TGFbeta1, Tgfb, Tgfb-1}, Il10 (interleukin 10) [NCBI Gene 16153] {aka CSIF, If2a, Il-10}, Il4 (interleukin 4) [NCBI Gene 16189] {aka BSF-1, Il-4}, Il5 (interleukin 5) [NCBI Gene 16191] {aka Il-5}
- **Diseases:** lung inflammation (MESH:D011014), Asthma (MESH:D001249), inflammation (MESH:D007249), pathological (MESH:D005598)
- **Chemicals:** MDA (MESH:D008315), Hydrogen (MESH:D006859)
- **Species:** Mus musculus (house mouse, species) [taxon 10090]

## Full text

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## Figures

5 figures with captions in the complete paper: https://tomesphere.com/paper/PMC12560338/full.md

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Source: https://tomesphere.com/paper/PMC12560338