222 The role of IL-5 and TGF-betal in eosinophilic inflammation in nasal polyps

Cytokine Profiles in Nasal Fluid in Patients with Nasal Polyps: A Flow Cytometric StudyBiological markers in nasal fluid provide valuable information on nasal pathophysiology. The aims of this study were to compare the cytokine profiles of nasal fluid in subjects with nasal polyps (NP) and co-morbid asthma and NP patients without asthma and to determine the role of these cytokines in the development of NP. Thirty patients with NP (15 asthmatic and 15 non asthmatic) were included in this prospective study. Nasal secretion samples were collected from nasal cavities of all 30 subjects. The levels of eleven cytokines (TNF-α, TNF-β, IL-1β, IL-2, IL-4, IL-5, IL-6, IL-8, IL-10, IL-12, and IFN-γ) were measured using flow cytometry. The concentrations of Th2 cytokines IL-5, IL-6 and IL-10 were significantly higher in patients with NP and asthma compared with subjects with NP without asthma. We also found significantly higher levels of IFN-α, IL-4, IL-6 and IL-10 in allergic patients with NP and asthma compared with those without asthma. In nonallergic patients with NP and asthma, the concentrations of TNF-α, IL-5 and IL-6 were significantly higher than in nonallergic patients with NP without asthma. Our results show that the presence of Th2 cytokines, especially IL-5 and IL-6 in patients with NP and asthma is a more prominent feature than in those without asthma that relates to the increased eosinophilic inflammation. We have also found a significant influence of allergy on the cytokine profiles both in asthmatic and nonasthmatic patients.

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Aspirin exacerbated respiratory disease: Role of periostin in Brazilian patients with chronic rhinosinusitis and nasal polyps

10.26226/morressier.5b0a2cfdd4cd1a00196f780e ◽

2018 ◽

Author(s):

Daniel Loiola Cordeiro

Keyword(s):

Chronic Rhinosinusitis ◽

Respiratory Disease ◽

Nasal Polyps ◽

Aspirin Exacerbated Respiratory Disease

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Faculty Opinions recommendation of Pathogenesis of chronic rhinosinusitis with nasal polyps: role of IL-6 in airway epithelial cell dysfunction.

Faculty Opinions – Post-Publication Peer Review of the Biomedical Literature ◽

10.3410/f.737631789.793574485 ◽

2020 ◽

Author(s):

Devyani Lal ◽

Shilpika Bajpai

Keyword(s):

Epithelial Cell ◽

Chronic Rhinosinusitis ◽

Nasal Polyps ◽

Airway Epithelial Cell ◽

Airway Epithelial ◽

Cell Dysfunction

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Let-7a-5p regulates the inflammatory response in chronic rhinosinusitis with nasal polyps

Diagnostic Pathology ◽

10.1186/s13000-021-01089-0 ◽

2021 ◽

Vol 16 (1) ◽

Author(s):

Jianwei Zhang ◽

Lei Han ◽

Feng Chen

Keyword(s):

Inflammatory Response ◽

Chronic Rhinosinusitis ◽

Nasal Polyps ◽

Mapk Pathway ◽

Inhibitory Effect ◽

Luciferase Reporter ◽

Western Blot Assay ◽

Protein Levels ◽

Tnf Α

Abstract Background Let-7a-5p is demonstrated to be a tumor inhibitor in nasopharyngeal carcinoma. However, the role of let-7a-5p in chronic rhinosinusitis with nasal polyps (CRSwNP) has not been reported. This study is designed to determine the pattern of expression and role of let-7a-5p in CRSwNP. Methods The expression level of let-7a-5p, TNF-α, IL-1β, and IL-6 in CRSwNP tissues and cells were detected by RT-qPCR. Western blot assay was carried out to measure the protein expression of the Ras-MAPK pathway. Dual luciferase reporter assay and RNA pull-down assay were used to explore the relationship between let-7a-5p and IL-6. Results Let-7a-5p was significantly downregulated in CRSwNP tissues and cells. Moreover, the mRNA expression of TNF-α, IL-1β and IL-6 was increased in CRSwNP tissues, while let-7a-5p mimic inhibited the expression of TNF-α, IL-1β and IL-6. Besides that, let-7a-5p was negatively correlated with TNF-α, IL-1β and IL-6 in CRSwNP tissues. In our study, IL-6 was found to be a target gene of let-7a-5p. Additionally, let-7-5p mimic obviously reduced the protein levels of Ras, p-Raf1, p-MEK1 and p-ERK1/2, while IL-6 overexpression destroyed the inhibitory effect of let-7a-5p on the Ras-MAPK pathway in CRSwNP. Conclusion We demonstrated that let-7a-5p/IL-6 interaction regulated the inflammatory response through the Ras-MAPK pathway in CRSwNP.

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The Role of CD68 (+) Histiocytic Macrophages in Nasal Polyp Development

Journal of Neurological Surgery Part B Skull Base ◽

10.1055/s-0040-1715593 ◽

2020 ◽

Author(s):

Nuray Bayar Muluk ◽

Osman Kürşat Arikan ◽

Pınar Atasoy ◽

Rahmi Kiliç ◽

Eda Tuna Yalçinozan

Keyword(s):

Nasal Cavity ◽

Nasal Polyp ◽

Nasal Polyps ◽

Deep Layer ◽

Ethmoid Sinus ◽

Adult Patients ◽

Control Group ◽

Study Group ◽

Deep Layers

Abstract Objectives The aim of this study was to investigate the role of CD68 (+) histiocytic macrophages (H-M) in the nasal polyp pathogenesis. Materials and Methods The study group consisted of 24 adult patients with nasal polyposis. The control group consisted of 11 adult patients without nasal polyps. A total of 36 nasal polyp samples (10-nasal cavity, 10-maxillary sinus, and 16-ethmoid sinus) from the study group and 11 inferior turbinate samples from the control group were analyzed by immunohistochemical staining, with monoclonal antibodies against CD68 (+) H-M. Results CD68 positivity was significantly higher than the control group in the subepithelial (SE) layer of the ethmoid sinus, and deep layers of nasal cavity, maxillary, and ethmoid sinuses. In SE and deep layers of ethmoid and maxillary sinuses, CD68 positivity was significantly higher than that of the epithelial layer. In the deep layer, histiocytic macrophages tended to gather around eosinophils. Conclusion The high numbers of CD68 (+) histiocytic macrophages mainly located in deep layer of lamina propria may be responsible for the phagocytosis of eosinophils within the polyp tissue. Therefore, it may be concluded that increased macrophages in nasal polyps do not trigger the growth of nasal polyps. Instead, they may serve to reduce the number of eosinophils in already-developed nasal polyps.

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