Role of IFN-γ, IL-13, and IL-17 on mucociliary differentiation of nasal epithelial cells in chronic rhinosinusitis with nasal polyps

2016 ◽  
Vol 46 (3) ◽  
pp. 449-460 ◽  
Author(s):  
J. Jiao ◽  
S. Duan ◽  
N. Meng ◽  
Y. Li ◽  
E. Fan ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Chronic Rhinosinusitis ◽  
Nasal Polyps ◽  
Nasal Epithelial Cells ◽  
Ifn Γ ◽  
Mucociliary Differentiation

The Expression and Regulation of Na+-K+-ATPase in Nasal Epithelial Cells of Chronic Rhinosinusitis with Nasal Polyps

ORL ◽  
2021 ◽  
pp. 1-8
Author(s):  
Guangyi Ba ◽  
Ru Tang ◽  
Song Mao ◽  
Zhipeng Li ◽  
Haibo Ye ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Chronic Rhinosinusitis ◽  
Nasal Polyps ◽  
Cell Permeability ◽  
Mrna Levels ◽  
Nasal Epithelial Cells ◽  
Protein Levels ◽  
Control Subjects ◽  
Human Nasal Epithelial Cells ◽  
Ifn Γ

<b><i>Objective:</i></b> Na<sup>+</sup>-K<sup>+</sup>-ATPase (NKA) is essential in maintaining cell permeability, reserving potential energy, and preventing cellular edema. Nevertheless, how NKA expression is altered and regulated in chronic rhinosinusitis with nasal polyps (CRSwNPs) remain uncertain. Therefore, the present study aimed to explore the expression and regulation of NKA in CRSwNP. <b><i>Methods:</i></b> NKA immunolabeling was assessed by the immunohistochemistry method, NKA protein levels were detected with the Western blotting method, and mRNA levels of NKA and aquaporin-5 (AQP5) were assayed by real-time PCR in nasal tissues from CRSwNP and control subjects. The co-localization of NKA with inflammatory cells was evaluated by immunofluorescence staining. In addition, human nasal epithelial cells (HNECs) were cultured and stimulated using various stimulators to evaluate the regulation of NKA. <b><i>Results:</i></b> We found significantly decreased NKA positive cells, NKA protein levels, and mRNA levels of NKA and AQP5 in nasal tissues from CRSwNP patients compared to control subjects, especially in eosinophilic CRSwNP. Furthermore, NKA mRNA levels in HNECs were downregulated by staphylococcal enterotoxin B (SEB), lipopolysaccharides (LPSs), inflammatory cytokine (IFN)-γ, IL-4, IL-13, and IL-1β. <b><i>Conclusion:</i></b> NKA and AQP5 expressions were decreased in CRSwNP. NKA in HNECs could be suppressed by SEB, LPS, IFN-γ, IL-4, IL-13, and IL-1β. Impairment of NKA may contribute to the genesis and development of CRSwNP via inducing AQP5 downregulation and edema.

scholarly journals Hypomethylation of the IL8 promoter in nasal epithelial cells of patients with chronic rhinosinusitis with nasal polyps

2019 ◽  
Vol 144 (4) ◽  
pp. 993-1003.e12 ◽  
Author(s):  
Jingyun Li ◽  
Jian Jiao ◽  
Ming Wang ◽  
Yunbo Gao ◽  
Ying Li ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Chronic Rhinosinusitis ◽  
Nasal Polyps ◽  
Nasal Epithelial Cells

Macrolide Treatment Decreased the Size of Nasal Polyps and IL-8 Levels in Nasal Lavage

2000 ◽  
Vol 14 (3) ◽  
pp. 143-148 ◽  
Author(s):  
Takechiyo Yamada ◽  
Shigeharu Fujieda ◽  
Shigehito Mori ◽  
Hideyuki Yamamoto ◽  
Hitoshi Saito
Keyword(s):  
Cystic Fibrosis ◽  
Epithelial Cells ◽  
Chronic Rhinosinusitis ◽  
Nasal Polyps ◽  
Experimental Studies ◽  
Nasal Lavage ◽  
Nasal Epithelial Cells ◽  
Diffuse Panbronchiolitis ◽  
Human Nasal Epithelial Cells

Recently, epidemiologic and experimental studies have been reported that long-term macrolides are effective for the treatment of chronic airway inflammatory diseases including diffuse panbronchiolitis, chronic rhinosinusitis, and cystic fibrosis (Jaffe A, Francis J, Rosenthal M, et al. Long-term azithromycin may improve lung function in children with cystic fibrosis. Lancet 351:420, 1998), and that macrolides can directly reduce the production of IL-8 by nasal epithelial cells (Suzuki H, Shimomura A, Ikeda K, et al. Inhibitory effect of macrolides on interleukin-8 secretion from cultured human nasal epithelial cells. Laryngoscope 107:1661–1666, 1997). In this study we administered macrolides with 14-membered rings to patients with nasal polyps due to chronic rhinosinusitis for at least 3 months and measured the IL-8 level in nasal lavage from those patients. The IL-8 levels in nasal lavage from patients with nasal polyps were reduced during macrolide treatment. There was significant correlation between decreased IL-8 levels in nasal lavage and the clinical effect of macrolides on the size of the nasal polyps. In the group whose polyps were reduced in size, the IL-8 levels dramatically decreased from 231.2 pg/mL to 44.0 pg/mL (p < 0.05), and were significantly higher before macrolide treatment than those in the group whose polyps showed no change (p < 0.005). This reduction in IL-8 may be an important aspect of the effect of macrolide treatment on nasal polyps in chronic rhinosinusitis.

scholarly journals S100A8 Enhances IL-1β Production from Nasal Epithelial Cells in Eosinophilic Chronic Rhinosinusitis

2021 ◽  
Author(s):  
Ayaka Nakatani ◽  
Takeshi Tsuda ◽  
Yohei Maeda ◽  
Masaki Hayama ◽  
Daisuke Okuzaki ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Chronic Rhinosinusitis ◽  
Nasal Polyps ◽  
Expression Profiles ◽  
Allergic Inflammation ◽  
Gene Expression Profiles ◽  
Interleukin 1Β ◽  
Nasal Epithelial Cells ◽  
Human Nasal Epithelial Cells ◽  
Eosinophilic Chronic Rhinosinusitis

Abstract Chronic rhinosinusitis is classified into eosinophilic chronic rhinosinusitis (ECRS) and non-eosinophilic chronic rhinosinusitis (NECRS). ECRS is a refractory allergic disease involving a variety of immune and epithelial cells. S100A8 is a damage-associated molecular pattern that is closely related to allergic inflammation. However, the pathological implications of S100A8 in ECRS have not been clarified. We evaluated the role of S100A8 in the pathogenesis of ECRS. Gene expression profiles of nasal polyps obtained from patients with ECRS or NECRS were evaluated using RNA sequencing. S100A8 was identified as a significantly upregulated gene in nasal polyps associated with ECRS. Immunohistochemistry consistently revealed intense S100A8 staining in nasal polyps from patients with ECRS. Human nasal epithelial cells expressed the receptor for advanced glycation end products and Toll-like receptor 4. Recombinant S100A8 protein induced interleukin-1β secretion in human nasal epithelial cells. Our data demonstrate that S100A8 results in production of interleukin-1β in the nasal epithelium, which may be involved in the pathogenesis of ECRS.

Expression of TLR2 and TLR4 Messenger RNA in the Epithelial Cells of the Nasal Airway

2005 ◽  
Vol 19 (3) ◽  
pp. 236-239 ◽  
Author(s):  
Zhen Dong ◽  
Zhanquan Yang ◽  
Chengshuo Wang
Keyword(s):  
Epithelial Cells ◽  
Chronic Rhinosinusitis ◽  
Nasal Mucosa ◽  
Messenger Rna ◽  
Nasal Epithelial Cells ◽  
Tlr4 Mrna ◽  
Human Nasal Epithelial Cells ◽  
Local Host ◽  
Adult Volunteers

Background Epithelium of nasal mucosa is the first line of defense against invading pathogens. This study investigated the expression of Toll-like receptor (TLR) 2 and TLR4 in epithelial cells of nasal mucosa and understood the role of TLRs in the innate immunity of nasal mucosa. Methods Human nasal epithelial cells were obtained by scraping the middle one-third of inferior turbinates from 30 patients with chronic rhinosinusitis and 20 healthy adult volunteers. The epithelial cells are made into smears. In situ hybridization was performed for TLR2 and TLR4 messenger RNA (mRNA). Results TLR2 and TLR4 mRNA were expressed in the nasal epithelial cells. The expression of the two genes was significantly higher in the chronic rhinosinusitis group than in the normal control (TLR2, t = 8.605, p < 0.0005; TLR4, t = 9.050, p < 0.0005). Conclusion This study is the first to establish the presence of both TLR2 and TLR4 mRNA on epithelial cells of nasal mucosa, and their expression can be up-regulated in infectious conditions. These results show that TLR2 and TLR4 may play a important role in local host defense of nasal mucosa.

scholarly journals HSP70 Expression in Nasal Epithelial Cells in Patients with Chronic Rhinosinusitis with Nasal Polyps

2019 ◽  
Vol 29 (2) ◽  
pp. 166-166
Author(s):  
Anatolii Onishchenko ◽  
◽  
Anton Tkachenko ◽  
Elina Kharchenko ◽  
Diana Sklyaruk ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Chronic Rhinosinusitis ◽  
Nasal Polyps ◽  
Hsp70 Expression ◽  
Nasal Epithelial Cells

scholarly journals WDPCP Modulates Cilia Beating Through the MAPK/ERK Pathway in Chronic Rhinosinusitis With Nasal Polyps

2021 ◽  
Vol 8 ◽  
Author(s):  
Yun Ma ◽  
Peng Tian ◽  
Hua Zhong ◽  
Fan Wu ◽  
Qining Zhang ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Chronic Rhinosinusitis ◽  
Nasal Polyp ◽  
Nasal Polyps ◽  
Essential Element ◽  
Nasal Epithelium ◽  
Erk Pathway ◽  
Low Expression

Cilia loss and dysfunction is one of the typical pathological features of chronic rhinosinusitis with nasal polyps (CRSwNP). Tryptophan-aspartic acid (W-D) repeat containing planar cell polarity effector (WDPCP) has been proven to be an essential element for ciliogenesis in human nasal epithelium, but its role in the beating of cilia remains unclear. In this study, we sought to investigate the role of WDPCP and its underlying mechanism behind the dysfunction in the beating of cilia in nasal polyp tissue. We demonstrated WDPCP expression in the epithelium of nasal polyps. We also investigated the MAPK/ERK pathway in primary human sinonasal epithelial cells to explore the function of WDPCP. The air–liquid interface culture system was used as a model to verify the role of WDPCP and the MAPK/ERK pathway in the beating of cilia. With the dysfunction of cilia beating, we observed a low expression of WDPCP in the epithelium of nasal polyp tissues. Within the in vitro study, we found that WDPCP was critical for mitochondrial biogenesis and mitochondrial function in human sinonasal epithelial cells, possibly due to the activation of the MAPK/ERK pathway. The mitochondrial dysfunction caused by U0126 or lacking WDPCP could be partially recovered by dexamethasone. The low expression of WDPCP in nasal epithelium could affect mitochondria via the MAPK/ERK pathway, which may contribute to the dysfunction in the beating of cilia in CRSwNP.

scholarly journals WDPCP modulates cilia beating through MAPK/ERK pathway in chronic rhinosinusitis

2020 ◽  
Author(s):  
Yun Ma ◽  
Peng Tian ◽  
Hua Zhong ◽  
Fan Wu ◽  
Qining Zhang ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Chronic Rhinosinusitis ◽  
Nasal Polyps ◽  
Planar Cell Polarity ◽  
Essential Element ◽  
Nasal Epithelium ◽  
Erk Pathway ◽  
Low Expression

Abstract Background: Cilia loss and dysfunction is one of the typical pathological features of chronic rhinosinusitis. Tryptophan-aspartic acid (W-D) repeat containing planar cell polarity effector (WDPCP) has been proven to be an essential element for ciliogenesis in human nasal epithelium, but its role in the beating of cilia remains unclear. Cilia beating requires energy from the mitochondria, which is regulated by the MAPK/ERK pathway. In this study, we sought to investigate the role of WDPCP and its underlying mechanism behind the dysfunction in the beating of cilia in chronic rhinosinusitis.Methods: We demonstrated WDPCP expression in the epithelium of nasal polyps. We also investigated the MAPK/ERK pathway in primary human sinonasal epithelial cells to explore the function of WDPCP. The air-liquid interface culture system was used as a model to verify the role of WDPCP and the MAPK/ERK pathway in the beating of cilia.Results: With the dysfunction of cilia beating, we observed a low expression of WDPCP in the epithelium of nasal polyps. Within the in vitro study, we found that WDPCP was critical for mitochondrial biogenesis and mitochondrial function in human sinonasal epithelial cells, possibly due to the activation of the MAPK/ERK pathway. The mitochondrial dysfunction caused by U0126 or lacking WDPCP could be partially recovered by dexamethasone.Conclusion: The low expression of WDPCP in nasal epithelium could affect mitochondria via the MAPK/ERK pathway, which may contribute to the dysfunction in the beating of cilia in chronic rhinosinusitis.

scholarly journals Cytokine Signature and Involvement in Chronic Rhinosinusitis with Nasal Polyps

2021 ◽  
Vol 23 (1) ◽  
pp. 417
Author(s):  
Florent Carsuzaa ◽  
Émilie Béquignon ◽  
Xavier Dufour ◽  
Guillaume de Bonnecaze ◽  
Jean-Claude Lecron ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Inflammatory Response ◽  
Chronic Rhinosinusitis ◽  
Inflammatory Cytokines ◽  
Nasal Polyps ◽  
Inflammatory Cells ◽  
Eosinophilic Infiltration ◽  
Th2 Cytokines ◽  
Current State

Cytokines are well known to play a central role in chronic rhinosinusitis with nasal polyps (CRSwNP), particularly in maintenance of the inflammatory response and the recruitment of eosinophils. The pathophysiological concepts concerning the involvement of inflammatory cytokines in CRSwNP have gradually evolved. Although the Th2 cytokines environment associated with an eosinophilic infiltration has retained a central role in the genesis of polyps, the role of other cytokine subpopulations has also and more recently been detailed, leading to a specific and complex signature in CRSwNP. The purpose of this review is to summarize the current state of knowledge about the cytokine signature in CRSwNP, the role of cytokines in the pathogenesis of this disease and in the intercellular dialog between epithelial cells, fibroblasts and inflammatory cells. Knowledge of this precise cytokine signature in CRSwNP is fundamental in the perspective of potential targeting biotherapies.

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