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Environmental allergens house dust mite-induced asthma is associated with ferroptosis in the lungs
Weifeng Tang1,2, Ming Dong3, Fangzhou Teng1,2
1Department of Integrative Medicine, Huashan Hospital, Fudan University, Shanghai 200040, P.R. China.
Abstract:
Previous studies have indicated that allergens such as house dust mites (HDM) in the environment can induce allergic asthma. Ferroptosis is a newly discovered form of regulatory cell death characterized by aberrant lipid peroxidation and the accumulation of reactive oxygen species (ROS) in cells. However, whether ferroptosis participates in the pathological process of asthma remains to be elucidated. The present study used a HDM-induced mouse asthma model to determine the effect of HDM exposure on allergic asthma and its underlying mechanisms. Female BALB/c mice were intranasally exposed to HDM to induce allergic asthma. Airway hyperresponsiveness (AHR), lung inflammation, mucus secretion, IgE levels, cytokine levels and inflammatory cell counts in bronchoalveolar lavage fluid (BALF) were investigated. In addition, the morphological changes of mitochondria, ROS levels, glutathione (GSH) levels and changes in ferroptosis pathway proteins were also determined in murine lungs. As a result, HDM exposure significantly increased AHR, inflammatory cell infiltration and mucus secretion around the airways. Furthermore, elevated IgE levels in the BALF, lung eosinophilia and a concomitant increase in IL-13 and IL-5 levels in BALF were observed. HDM inhalation increased ROS and decreased GSH levels in the lungs. HDM inhalation induced dysmorphic small mitochondria with decreased crista, as well as condensed, ruptured outer membranes. Western blotting demonstrated that the activities of glutathione peroxidase 4 and catalytic subunit solute carrier family 7 member 11 were significantly decreased, and that protein expression levels of acyl-CoA synthetase long-chain family member 4 and 15 lipoxygenase 1 were upregulated compared with mice in the normal control group. Overall, these results indicated that the AHR, airway inflammation, lipid peroxidation and ROS levels increased in HDM-induced asthma, and that HDM inhalation induced ferroptosis in the lungs, which helped to form an improved understanding of the pathogenesis of allergic asthma.
Insights
House dust mite exposure triggers allergic asthma by inducing ferroptosis, a cell death pathway involving lipid peroxidation and reactive oxygen species (ROS). This study reveals ferroptosis
Area of Science:
- Immunology
- Cell Biology
- Respiratory Medicine
Background:
- Allergic asthma is often induced by environmental allergens like house dust mites (HDM).
- Ferroptosis, a cell death form marked by lipid peroxidation and reactive oxygen species (ROS), is a recent discovery.
- The role of ferroptosis in asthma pathogenesis remains unclear.
Purpose of the Study:
- To investigate the effects of HDM exposure on allergic asthma.
- To elucidate the underlying mechanisms, focusing on ferroptosis in HDM-induced asthma.
Main Methods:
- A mouse model of HDM-induced allergic asthma was established.
- Evaluated airway hyperresponsiveness (AHR), lung inflammation, mucus secretion, IgE, and cytokine levels.
- Assessed mitochondrial morphology, ROS, glutathione (GSH), and ferroptosis-related proteins.
Main Results:
- HDM exposure significantly increased AHR, airway inflammation, mucus production, IgE, IL-13, and IL-5 levels.
- HDM inhalation led to increased ROS, decreased GSH, and characteristic ferroptotic mitochondrial damage.
- Key ferroptosis regulators, including glutathione peroxidase 4, were downregulated, while others were upregulated.
Conclusions:
- HDM-induced asthma involves increased AHR, inflammation, lipid peroxidation, and ROS.
- HDM inhalation triggers ferroptosis in the lungs, contributing to allergic asthma pathogenesis.
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