ArticleJournal of leukocyte biology2022
Hemin-primed dendritic cells suppress allergic airway inflammation through releasing extracellular vesicles.
Article in Journal of leukocyte biology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 9 citations in OpenAlex.
- Extracellular Vesicles from Monocyte-Derived Dendritic Cells Modulate Lymphocyte and Eosinophil Responses in Cow's Milk Allergy.International journal of molecular sciences · 2026Article
- Investigating the causal association between heme oxygenase-1 and asthma: A bidirectional two-sample Mendelian randomization analysis in a European population.The World Allergy Organization journal · 2024Article
- Recent advances in extracellular vesicle engineering and its applications to regenerative medicine.Biomaterials research · 2023Review
- Tolerogenic dendritic cells in radiation-induced lung injury.Frontiers in immunology · 2023Review
- Recent Advances in Nanomaterials for Asthma Treatment.International journal of molecular sciences · 2022Review
- Hemin-primed dendritic cells suppress allergic airway inflammation through releasing extracellular vesicles.Journal of leukocyte biology · 2022Article
- Immune Regulation of Heme Oxygenase-1 in Allergic Airway Inflammation.Antioxidants (Basel, Switzerland) · 2022Review
- Crosstalk between ILC2s and Th2 CD4Journal of immunology research · 2022Review
- Packaging and Delivery of Asthma Therapeutics.Pharmaceutics · 2021Review
Corrections and comments
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Authors and funding
8 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Hemin, a substrate of heme oxygenase (HO)-1, induces HO-1 expression on a variety of cells to exert anti-oxidant and anti-inflammatory roles. However, the role of HO-1 in allergic diseases for dendritic cells (DCs) is not fully understood. Here, we report that HO-1 modulates asthmatic airway inflammation by hemin-treated DC-released extracellular vesicles (DCEVs). Following induction of bone marrow-derived DCs by hemin and then by house dust mite (HDM) in vitro, mouse CD4+ naïve T cells were cocultured with DCEVs to determine T helper (h) cell differentiation. C57BL/6 mice were sensitized by different stimuli-induced DCEVs and challenged with HDM to analyze the changes of inflammatory cells and cytokines in the lung and bronchoalveolar lavage fluid. The results showed that hemin-treated DCEVs (hemin-DCEVs) express phosphatidylserine (PS), CD81, heat shock protein 70, and HO-1, which facilitates regulatory T (Treg) cells differentiation in vitro and in vivo. In HDM-induced asthmatic mouse model, hemin-DCEVs inhalation reduced eosinophils infiltration and mucus secretion in the airway, decreased the levels of IL-4, IL-5, and IL-13 in the lung and the number of Th2 cells in mediastinal lymph nodes (MLNs), and increased the number of Treg cells in MLNs. Thus, our study demonstrated, for the first time, that EVs from HO-1-overexpressing DCs alleviate allergic airway inflammation of eosinophilic asthma by potentiating Treg cells differentiation and limiting proinflammatory cytokine secretion, which expands our understanding of HO-1 function, opening the door for HO-1 inducer-like hemin as a novel therapeutic strategy for asthma or other allergic diseases.
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Registered trials
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