Hop Water Extract Inhibits Double-stranded RNA-induced Thymic Stromal Lymphopoietin Release from Human Nasal Epithelial Cells

2012 ◽  
Vol 26 (6) ◽  
pp. 433-438 ◽  
Author(s):  
Jun Fuchimoto ◽  
Takashi Kojima ◽  
Naoyuki Kobayashi ◽  
Tsuyoshi Ohkuni ◽  
Noriko Ogasawara ◽  
...  
Keyword(s):  
Allergic Rhinitis ◽  
Epithelial Cells ◽  
Water Extract ◽  
Thymic Stromal Lymphopoietin ◽  
Poly I:C ◽  
Dependent Manner ◽  
Double Stranded Rna ◽  
Nasal Epithelial Cells ◽  
Polycytidylic Acid ◽  
Human Nasal Epithelial Cells

Background Thymic stromal lymphopoietin (TSLP) acts as a master switch for allergic inflammation and plays a key role in allergic diseases, including allergic rhinitis. Double-stranded RNA (dsRNA) recognized by Toll-like receptor 3 (TLR3) strongly activates TSLP release from human human nasal epithelial cells (HNECs). Hop (Humulus lupulus L.) extracts have been shown to have potent pharmacologic effects on inflammation. Methods To investigate whether a hop water extract (HWE) prevents TSLP release from HNECs, human telomeras reverse transcriptase (hTERT)-transfected HNECs, used as a model of normal HNECs, were pretreated with HWE before treatment with the TLR3 ligand Polyinosine-polycytidylic acid (poly[I:C]). Results In the hTERT-transfected HNECs, treatment with HWE significantly reduced poly(I:C)-induced production and release of TSLP in a dose-dependent manner, as well as dexamethasone. Treatment with the protein kinase C (PKC) inhibitor GF109203X and NF-κB inhibitor IMD-0354 also reduced poly(I:C)-induced TSLP release from hTERT-transfected HNECs. Treatment with HWE efficiently prevented up-regulation of PKC activity by 12-O-tetradecanoyl phorbol-13-acetate but not NF-κB activity induced by IL-1β in hTERT-transfected HNECs. Conclusion Our results clearly indicated that HWE inhibited dsRNA-induced production and release of TSLP via a PKC signal pathway in HNECs and it may have potent preventive effects against allergic rhinitis.

Effects of IL-1β, TNF-α, and TGF-β on Proliferation of Human Nasal Epithelial Cells in Vitro

1998 ◽  
Vol 12 (4) ◽  
pp. 279-282 ◽  
Author(s):  
Yang-Gi Min ◽  
Chae-Seo Rhee ◽  
Sam-Hyun Kwon ◽  
Kang Soo Lee ◽  
Ja Bock Yun
Keyword(s):  
Epithelial Cells ◽  
Collagen Gel ◽  
Time Dependent ◽  
Dependent Manner ◽  
Primary Cells ◽  
Nasal Epithelial Cells ◽  
Human Nasal Epithelial Cells ◽  
Tnf Α ◽  
Collagen Gel Matrix

Previous reports suggest that cytokines may be involved in proliferation of the epithelium. The aim of this study was to determine the effects of cytokines, IL-1β, TNF-α, and TGF-β on proliferation of human nasal epithelial cells (HNECs) in vitro. Primary cells were cultured from HNECs on collagen gel matrix. Subcultured HNECs were incubated in a medium with recombinant human (rh) cytokines, rhIL-1β, rhTNF-a, and rhTGF-β at different concentrations of 0.01 ng/mL, 0.1 ng/mL, 1 ng/mL, 10 ng/mL, and 100 ng/mL. After 2-day incubation with these cytokines, daily cell proliferation was measured by MTT assay for 6 days. While rhIL-1β inhibited proliferation of HNECs in concentration-dependent and time-dependent manners, rhTNF-a stimulated HNEC growth at concentrations ranging from 0.01 ng/mL to 10 ng/mL in concentration-dependent and time-dependent manner. In contrast, rhTGF-b inhibited HNEC growth irrespective of concentration and incubation time. This study suggests that IL-1β, TNF-α, and TGF-β may have an important role in the repair of the nasal mucosa by regulating proliferation of the nasal epithelium.

scholarly journals Daidzein-Stimulated Increase in the Ciliary Beating Amplitude via an [Cl−]i Decrease in Ciliated Human Nasal Epithelial Cells

2018 ◽  
Vol 19 (12) ◽  
pp. 3754 ◽  
Author(s):  
Taka-aki Inui ◽  
Makoto Yasuda ◽  
Shigeru Hirano ◽  
Yukiko Ikeuchi ◽  
Haruka Kogiso ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Beat Frequency ◽  
Cell Sheet ◽  
Ciliary Beat Frequency ◽  
Dependent Manner ◽  
Nasal Epithelial Cells ◽  
Ciliary Beating ◽  
Human Nasal Epithelial Cells ◽  
Cl Channels ◽  
Ciliary Beat

The effects of the isoflavone daidzein on the ciliary beat distance (CBD, which is a parameter assessing the amplitude of ciliary beating) and the ciliary beat frequency (CBF) were examined in ciliated human nasal epithelial cells (cHNECs) in primary culture. Daidzein decreased [Cl−]i and enhanced CBD in cHNECs. The CBD increase that was stimulated by daidzein was mimicked by Cl−-free NO3− solution and bumetanide (an inhibitor of Na+/K+/2Cl− cotransport), both of which decreased [Cl−]i. Moreover, the CBD increase was inhibited by 5-Nitro-2-(3-phenylpropylamino)benzoic acid (NPPB, a Cl− channel blocker), which increased [Cl−]i. CBF was also decreased by NPPB. The rate of [Cl−]i decrease evoked by Cl−-free NO3− solution was enhanced by daidzein. These results suggest that daidzein activates Cl− channels in cHNECs. Moreover, daidzein enhanced the microbead transport driven by beating cilia in the cell sheet of cHNECs, suggesting that an increase in CBD enhances ciliary transport. An [Cl−]i decrease enhanced CBD, but not CBF, in cHNECs at 37 °C, although it enhanced both at 25 °C. Intracellular Cl− affects both CBD and CBF in a temperature-dependent manner. In conclusion, daidzein, which activates Cl− channels to decrease [Cl−]i, stimulated CBD increase in cHNECs at 37 °C. CBD is a crucial factor that can increase ciliary transport in the airways under physiological conditions.

scholarly journals The Effect of IL-35 on the Expression of Nasal Epithelial-Derived Proinflammatory Cytokines

2021 ◽  
Vol 2021 ◽  
pp. 1-7
Author(s):  
Mingrong Nie ◽  
Qingxiang Zeng ◽  
Luo Xi ◽  
Yiquan Tang ◽  
Renzhong Luo ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Proinflammatory Cytokines ◽  
Lavage Fluid ◽  
Dermatophagoides Pteronyssinus ◽  
Poly I:C ◽  
Enzyme Linked Immunosorbent Assay ◽  
Nasal Epithelial Cells ◽  
Human Nasal Epithelial Cells ◽  
Baseline Levels

Background. Airway epithelium plays an important role during the development of allergic rhinitis (AR), which is characterized by production of thymic stromal lymphopoietin (TSLP), interleukin 33 (IL-33), and interleukin 25 (IL-25). IL-35, mainly expressed by Treg cells, have negative regulation in Th2, Th17, and ILC2 inflammation. However, the effect of IL-35 on human nasal epithelial cells (HNECs) especially the secretion of nasal epithelial-derived proinflammatory cytokines as well as the possible mechanism is still unclear. Methods. HNECs were cultured and stimulated by various stimulators. The expression of IL-33, IL-25, TSLP, eotaxin-1, eotaxin-2, and eotaxin-3 from supernatant was measured using real-time reverse transcription-polymerase chain reaction (RT-PCR) and enzyme-linked immunosorbent assay (ELISA). AR mice were developed to verify the effect of IL-35 on nasal epithelial cells in vivo. Results. After Poly I:C stimulation, IL-35 inhibited the production of IL-25, and TSLP from HNECs increased significantly compared with baseline levels ( P < 0.05 ). After Dermatophagoides pteronyssinus or Aspergillus fumigatus stimulation, IL-35 inhibited the production of IL-25, IL-33, and TSLP from HNECs increased significantly compared with baseline levels ( P < 0.05 ). After Dermatophagoides pteronyssinus, IL-35 inhibited the production of eotaxin-1, eotaxin-2, and eotaxin-3 released from HNECs increased significantly compared with baseline levels ( P < 0.05 ). Similarly, IL-35-treated AR mice presented with decreased expression of IL-33, IL-25, TSLP, eotaxin-1, eotaxin-2, and eotaxin-3 in nasal lavage fluid. Conclusion. IL-35 suppressed both type 2 inflammation-inducing cytokines and eosinophil chemotactic factor from HNECs, suggesting the important role of IL-35 during the development of AR.

Thymic stromal lymphopoietin enhances tight-junction barrier function of human nasal epithelial cells

2009 ◽  
Vol 338 (2) ◽  
pp. 283-293 ◽  
Author(s):  
Ryuta Kamekura ◽  
Takashi Kojima ◽  
Jun-ichi Koizumi ◽  
Noriko Ogasawara ◽  
Makoto Kurose ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Tight Junction ◽  
Barrier Function ◽  
Thymic Stromal Lymphopoietin ◽  
Nasal Epithelial Cells ◽  
Human Nasal Epithelial Cells

scholarly journals Fluticasone Propionate Suppresses Poly(I:C)-Induced ACE2 in Primary Human Nasal Epithelial Cells

2021 ◽  
Vol 11 ◽  
Author(s):  
Akira Nakazono ◽  
Yuji Nakamaru ◽  
Mahnaz Ramezanpour ◽  
Takeshi Kondo ◽  
Masashi Watanabe ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Fluticasone Propionate ◽  
Nasal Mucosa ◽  
Fold Change ◽  
Innate Immune ◽  
Cell Entry ◽  
Poly I:C ◽  
Nasal Epithelial Cells ◽  
Tlr Agonists ◽  
Human Nasal Epithelial Cells

BackgroundFrom the first detection in 2019, SARS-CoV-2 infections have spread rapidly worldwide and have been proven to cause an urgent and important health problem. SARS-CoV-2 cell entry depends on two proteins present on the surface of host cells, angiotensin-converting enzyme 2 (ACE2) and transmembrane protease serine 2 (TMPRSS2). The nasal cavity is thought to be one of the initial sites of infection and a possible reservoir for dissemination within and between individuals. However, it is not known how the expression of these genes is regulated in the nasal mucosa.ObjectiveIn this study, we examined whether the expression of ACE2 and TMPRSS2 is affected by innate immune signals in the nasal mucosa. We also investigated how fluticasone propionate (FP), a corticosteroid used as an intranasal steroid spray, affects the gene expression.MethodsPrimary human nasal epithelial cells (HNECs) were collected from the nasal mucosa and incubated with Toll-like receptor (TLR) agonists and/or fluticasone propionate (FP), followed by quantitative PCR, immunofluorescence, and immunoblot analyses.ResultsAmong the TLR agonists, the TLR3 agonist Poly(I:C) significantly increased ACE2 and TMPRSS2 mRNA expression in HNECs (ACE2 36.212±11.600-fold change, p&lt;0.0001; TMPRSS2 5.598±2.434-fold change, p=0.031). The ACE2 protein level was also increased with Poly(I:C) stimulation (2.884±0.505-fold change, p=0.003). The Poly(I:C)-induced ACE2 expression was suppressed by co-incubation with FP (0.405±0.312-fold change, p=0.044).ConclusionThe activation of innate immune signals via TLR3 promotes the expression of genes related to SARS-CoV2 cell entry in the nasal mucosa, although this expression is suppressed in the presence of FP. Further studies are required to evaluate whether FP suppresses SARS-CoV-2 viral cell entry.

scholarly journals MicroRNA-29a promotes the proliferation of human nasal epithelial cells and inhibits their apoptosis and promotes the development of allergic rhinitis by down-regulating FOS expression

PLoS ONE ◽  
2021 ◽  
Vol 16 (8) ◽  
pp. e0255480
Author(s):  
Yuqin Fan ◽  
Zhiyuan Tang ◽  
Jie Sun ◽  
Xiaorui Zhao ◽  
Zhen Li ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Allergic Rhinitis ◽  
Epithelial Cells ◽  
Cell Apoptosis ◽  
Luciferase Reporter ◽  
Nasal Epithelial Cells ◽  
Over Expression ◽  
Human Nasal Epithelial Cells ◽  
Gene Assay ◽  
Fos Expression

Objective To explore the regulation of microRNA-29a (miR-29a) on FOS in human nasal epithelial cells and its molecular mechanism, as well as the effects of miR-29a on the cell proliferation and apoptosis. Methods By cell transfection, gene silencing, quantitative real-time polymerase chain reaction (qRT-PCR), flow cytometry and TUNEL assay (for cell apoptosis), CCK-8 assay (for cell proliferation), dual-luciferase reporter gene assay and Western Blot, it was validated that miR-29a promoted the proliferation of human nasal epithelial cells and inhibited their apoptosis by down-regulating FOS expression in RPMI2650 and HNEpC cell lines. Results ①Compared with healthy controls, miR-29a expression was up-regulated and FOS mRNA expression was down-regulated in the nasal tissues from the patients with allergic rhinitis (AR). ②MiR-29a over-expression promoted the proliferation of RPMI2650 cells and HNEpC cells but inhibited their apoptosis. ③MiR-29a targeted at FOS. ④MiR-29a over-expression and FOS silencing both significantly promoted cell proliferation and inhibited cell apoptosis. After transfection with both miR-29a and FOS, there was a decrease in the proliferation but an increase in the apoptosis of cells.⑤MiR-29a promoted the proliferation of human nasal epithelial cells and inhibited their apoptosis by down-regulating FOS expression. Conclusion MiR-29a-/FOS axis can be regarded as a potential marker and a new therapy for AR.

Poly(I:C) reduces expression of JAM-A and induces secretion of IL-8 and TNF-α via distinct NF-κB pathways in human nasal epithelial cells

2011 ◽  
Vol 250 (1) ◽  
pp. 29-38 ◽  
Author(s):  
Tsuyoshi Ohkuni ◽  
Takashi Kojima ◽  
Noriko Ogasawara ◽  
Tomoyuki Masaki ◽  
Jun Fuchimoto ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Poly I:C ◽  
Nasal Epithelial Cells ◽  
Human Nasal Epithelial Cells ◽  
Tnf Α
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