ArticleJournal of inflammation research2022
CCL20/CCR6 Mediated Macrophage Activation and Polarization Can Promote Adenoid Epithelial Inflammation in Adenoid Hypertrophy.
Article in Journal of inflammation research, 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, 15 citations in OpenAlex.
- Sulf1 regulates inflammation via modulation of TGF-β dependent epicardial activation.EMBO reports · 2026Article
- The Association of Allergic Rhinitis with Chronic Adenotonsillar Diseases and Chronic Rhinosinusitis: A Mendelian Randomization Study.Combinatorial chemistry & high throughput screening · 2026Article
- A rat model of adenoid hypertrophy constructed by using ovalbumin and lipopolysaccharides to induce allergy, chronic inflammation, and chronic intermittent hypoxia.Animal models and experimental medicine · 2025Article
- CCL20 Expression via AKT-ERK1/2-AP1 Pathway inJournal of inflammation research · 2025Article
- Using Olink Proteomics to Identify Inflammatory Biomarkers in the Cerebrospinal Fluid in Guillain-Barré Syndrome.Journal of inflammation research · 2025Article
- Differentiating early-stage nasopharyngeal carcinoma from adenoidal hypertrophy via SLC40A1 expression and developing a prognostic model for disease progression.American journal of cancer research · 2025Article
- A Proteomic Study Based on Home Quarantine Model Identifies NQO1 and Inflammation Pathways Involved in Adenoid Hypertrophy.Journal of inflammation research · 2025Article
- Impact of chitosan oligosaccharide on microbiota-metabolite-immune axis in natural aging.Frontiers in nutrition · 2025Article
- Inflammation and olfactory loss are associated with at least 139 medical conditions.Frontiers in molecular neuroscience · 2024Article
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background: Adenoid hypertrophy (AH) is a chronic or acute obstruction-related ailment of the upper respiratory tract that arises as an inflammatory response to exposure of bacteria, viruses or allergies. Activation and polarization of macrophages are key processes in inflammation-related disorders like AH and CCL20/CCR6 axis is a critical therapeutic target. Purpose: To determine that CCL20/CCR6 mediated macrophage activation and polarization can promote adenoid epithelial inflammation in AH. Methods: To support this claim, CCL20 and CCR6 expressions were studied in clinical AH samples. In addition, the expressions of cytokines such as TNF-α, IL-1β, IL-6, IL-17, IL-10 and TGF-β were analysed. In vitro, human adenoid epithelial cells were co-cultured with polarized THP-1 and T lymphocyte H9 cells to study the expressions of several inflammatory markers. Results: The expressions of M1 macrophage markers CD86 and IL-17 were significantly increased, whereas the expressions of M2 macrophage markers CD206 and FOXP3 were significantly decreased. The THP-1 cells were successfully polarized to M0, M1 and M2 macrophages. The survival of macrophages improved after 24 hr of induction and enhanced TGF-β expression was observed. The expressions of the inflammatory cytokines IL-6, TNF-α, IL-1β and CCL20 increased significantly. Conclusion: Collectively, these results suggest that the CCL20/CCR6 mediated macrophage activation and polarization into M1-type macrophages can promote adenoid epithelial inflammation in AH. Further studies are warranted to determine the roles of inflammatory markers in the pathophysiology of AH and identifying potential targets.
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