ArticleAllergy & rhinology (Providence, R.I.)2012
Relationships between IL-17A and macrophages or MUC5AC in eosinophilic chronic rhinosinusitis and proposed pathological significance.
Article in Allergy & rhinology (Providence, R.I.), 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 29 citations in OpenAlex.
- Evaluating antioxidant treatment approaches for eosinophilic chronic sinusitis.Frontiers in immunology · 2026Review
- Involvement of CD40-CD40L and ICOS-ICOSL in the development of chronic rhinosinusitis by targeting eosinophils.Frontiers in immunology · 2023Article
- Role of IL-17A in Chronic Rhinosinusitis With Nasal Polyp.Allergy, asthma & immunology research · 2020Article
- Interleukin-Mediated Pendrin Transcriptional Regulation in Airway and Esophageal Epithelia.International journal of molecular sciences · 2019Review
- Central Role of IL-23 and IL-17 Producing Eosinophils as Immunomodulatory Effector Cells in Acute Pulmonary Aspergillosis and Allergic Asthma.PLoS pathogens · 2017Article
- IL-17E (IL-25) and IL-17RB promote respiratory syncytial virus-induced pulmonary disease.Journal of leukocyte biology · 2014Article
- Increased expression of pendrin in eosinophilic chronic rhinosinusitis with nasal polyps.Brazilian journal of otorhinolaryngologyArticle
- Activation of STAT6 by intranasal allergens correlated with the development of eosinophilic chronic rhinosinusitis in a mouse model.International journal of immunopathology and pharmacologyArticle
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Recently, some researchers have reported that macrophages and neutrophils were related to severe asthma. Mucus hypersecretion and persistent airway inflammation result from increased expression of mucin gene (MUC5AC). Eosinophilic chronic rhinosinusitis (ECRS) is considered as intractable rhinosinusitis. From the viewpoint of "one way one disease," we examined whether ECRS is associated with infiltrating macrophages, neutrophils, their promotive factors, and MUC5AC. We examined 21 nasal polyps with CRS. Each specimen was fixed in 10% phosphate-buffered formalin, embedded in paraffin, processed routinely, and then prepared as semithin sections (3.5 μm). We immunohistochemically observed the macrophages by using CD68, neutrophils by using neutrophil elastase and the promotive factors, monocyte chemotactic protein (MCP) 1, IL-17A, and IL-8, in both ECRS and non-ECRS. The number of macrophages (CD68(+) cells), IL-17A, and MUC5AC(+) cells in ECRS were significantly greater than in non-ECRS. The mean number of MCP-1(+) cells in ECRS was greater than that in non-ECRS, but not significantly. There was a significant correlation in all cases between IL-17A and macrophages or MUC5AC(+) cells. Neither the numbers of neutrophils (positive cells for neutrophil elastase) nor the IL-8(+) cells showed any significant differences between ECRS and non-ECRS. Our study suggested that infiltrating macrophages, IL-17A and MUC5AC, as well as eosinophils could have roles in the development of ECRS.
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