ArticleRespiratory research2025
SERPINB10 promotes macrophage M2 polarization and airway inflammation in asthma.
Article in Respiratory research, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers, 1 of them a synthesis that pooled it.
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Who cites it
7 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Phagocytic aberrations in macrophages in asthma: a mechanistic systematic review integratingFrontiers in immunology · 2026Pooled it
- Integrated Immune, Epithelial and Lipid Pathways in NSAID-Exacerbated Respiratory Disease.Clinical and translational allergy · 2026Review
- M2 macrophage-derived small extracellular vesicles carrying canagliflozin attenuate experimental asthma.Drug delivery and translational research · 2026Article
- Paucigranulocytic Asthma in Aspirin-Hypersensitive Patients: Pleiotropic Regulation of Type 2 Biomarkers.Clinical and translational allergy · 2026Article
- Regulation of macrophage polarization in chronic airway inflammatory diseases: immune interactions, metabolic reprogramming, and beyond.Frontiers in immunology · 2026Review
- Multiomics and Machine Learning Reveal Distinct Immune-Metabolic Signatures and Diagnostic Biomarkers for Asthma Inflammatory Endotypes.ACS omega · 2025Article
- Chronic compression induces transcriptional, metabolic, and functional state changes in macrophages that recapitulate tumor-associated phenotypes.Frontiers in immunology · 2025Article
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Authors and funding
9 authors.
Funding
Abstract
backgroundMacrophage M2 polarization plays a critical role in type 2 airway inflammation in asthma. We previously reported that serine peptidase inhibitor, clade B, member 10 (SERPINB10) promotes airway eosinophilic inflammation in asthma.
objectiveTo investigate the role of SERPINB10 in macrophage M2 polarization and airway inflammation in asthma.
methodsThe expression of SERPINB10 was detected in bronchoalveolar lavage (BAL) cells from 15 control subjects and 36 asthma patients. Serpinb10 knockout mice and wild type mice were sensitized and challenged with ovalbumin (OVA). Macrophage polarization and airway inflammation were evaluated. An adoptive transfer experiment of Serpinb10-deficient macrophages to macrophage-depleted mice was performed to assess the effect of Serpinb10 deficiency in macrophages on the airway inflammation in the model. The role of SERPINB10 in the activation of IL-4 receptor (IL-4R) signaling pathway and macrophage M2 polarization was investigated in cell cultures.
resultsSERPINB10 expression was markedly elevated in BAL cells from asthmatic patients, and was significantly correlated with fractional exhaled nitric oxide and CD206, a marker for macrophage M2 polarization. In the OVA-induced allergic airway inflammation mouse model, Serpinb10 deficiency significantly inhibited airway inflammation, mucous cell metaplasia and airway hyperresponsiveness. Moreover, Serpinb10 deficiency suppressed the expression of M2 markers including Cd206, Arg1 in mouse lung tissues and the protein levels of M2 macrophage effector cytokines including Ccl17 and Ccl22 in BAL fluid. Adoptive transfer of Serpinb10-deficient bone marrow-derived macrophages (BMDMs) to wild type mice depleted macrophages significantly suppressed the airway inflammation and mucous cell metaplasia. Mechanistically, SERPINB10 suppresses the degradation of IL-4Rα in macrophages, thereby upregulating the phosphorylation of Stat6 and Akt and leading to macrophage M2 polarization.
conclusionsSERPINB10 promotes macrophage M2 polarization by suppressing IL-4Rα degradation and upregulating IL-4R signaling. SERPINB10 is a potential therapeutic target for asthma.
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