Asthma and Molecular Hydrogen
In asthma, hydrogen showed to minimize both stress due to ROS and inflammation. In inflammation induced by ovalbumin, inhaling H2 gas decreases the amount of white blood cells in the bronchial-alveolar lavage fluid (BALF) especially eosinophils. It also significantly lowers the number of inflammation inducing pro-factors in the plasma, increases the catalysis of superoxide dismutase enzyme, and decreases in degree or intensity in the levels of certain genes like MPO and MDA (Zhang N et al., 2018). Inhibition of two activated pathways of NFkB and Nrf2, hydrogen significantly reduces airway hyper-responsiveness and goblet cell hyperplasia, as well as the response by T-helper-type-2, and it also reduces levels of IL-4 and immune-globin E (IgE). These effects can be attributed to hydrogen’s ability to alleviate goblet cell hyperplasia.
The role of macrophages of alveoli in lungs, under normal circumstances, is to keep a respiratory tract free of cell debri, pathogens like bacteria, and other foreign factors. The capability of macrophages of alveoli to phagocytose, on the other hand, is greatly diminished in asthma patients. Hydrogen gas, when inhaled, has the effect of correcting the incorrect phagocytosis that was occurring . Additionally, H2 gas inhibits the restructuring of airways, that leads to long-lasting changes in the structure & function of the airway wall. These changes, in turn, lead to a gradual decline in functioning of lungs . In the type of asthma induced by ovalbumin, HRS suppresses the pathway of NFkB, which causes a substantial reduction in mucus-index, MUC5-AC, and VEGF expression. Additionally, there is a reduction in the amount of deposition of collagen . This significantly reduces the amount of modification that occurs in the passageways.
