ArticleInflammation research : official journal of the European Histamine Research Society ... [et al.]2024
Deficiency of INPP4A promotes M2 macrophage polarization in eosinophilic chronic rhinosinusitis with nasal polyps.
Article in Inflammation research : official journal of the European Histamine Research Society ... [et al.], 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed, 7 citations in OpenAlex.
- IL-Mediated Macrophage Polarization Axis: From Inflammatory Positive Feedback Loop to Precision Biomarkers and Therapeutic Targets for Allergic Rhinitis-A Narrative Review.Journal of asthma and allergy · 2026Review
- Efferocytosis failure in chronic rhinosinusitis with nasal polyps: receptor-level mechanisms of unresolved type 2 inflammation.Frontiers in immunology · 2026Review
- Regulation of macrophage polarization in chronic airway inflammatory diseases: immune interactions, metabolic reprogramming, and beyond.Frontiers in immunology · 2026Review
- Identification and Functional Analysis of a Key Gene in the CHH Gene Family for Glucose Metabolism in the Pacific White ShrimpInternational journal of molecular sciences · 2025Article
- The advance on pathophysiological mechanisms of type 2 chronic rhinosinusitis with nasal polyposis.Frontiers in allergy · 2025Review
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Authors and funding
10 authors at 1 institution in 1 country.
Funding
Abstract
objectiveThe treatment of eosinophilic chronic rhinosinusitis with nasal polyps (E-CRSwNP) remains a challenge due to its complex pathogenesis. Inositol polyphosphate-4-phosphatase type IA (INPP4A), a lipid phosphatase, has been implicated in allergic asthma. However, the expression and function of INPP4A in E-CRSwNP remain unclear. This study aims to investigate the role of INPP4A in macrophages in E-CRSwNP.
methodsWe assessed the expression of INPP4A in human and mouse nasal mucosal tissues via immunofluorescence staining. THP-1 cells were cultured and exposed to various cytokines to investigate the regulation of INPP4A expression and its functional role. Additionally, we established a murine nasal polyp (NP) model and administrated an INPP4A-overexpressing lentivirus evaluate its impact on NP.
resultsThe percentage of INPP4A + CD68 + macrophages among total macrophages decreased in the E-CRSwNP group compared to the control and the non-eosinophilic CRSwNP (NE-CRSwNP) groups, exhibiting an inverse correlation with an increased percentage of CD206 + CD68 + M2 macrophages among total macrophages. Overexpression of INPP4A led to a reduced percentage of THP-1 cells polarizing towards the M2 phenotype, accompanied by decreased levels of associated chemotactic factors including CCL18, CCL22, CCL24, and CCL26. We also validated the involvement of the PI3K-AKT pathway in the function of INPP4A in vitro. Furthermore, INPP4A overexpression in the murine NP model resulted in the attenuation of eosinophilic inflammation in the nasal mucosa.
conclusionsINPP4A deficiency promotes macrophage polarization towards the M2 phenotype, leading to the secretion of chemokines that recruit eosinophils and Th2 cells, thereby amplifying eosinophilic inflammation in E-CRSwNP. INPP4A may exert a suppressive role in eosinophilic inflammation and could potentially serve as a novel therapeutic strategy.
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