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.

scholarly journals Quercetin Enhances the Thioredoxin Production of Nasal Epithelial Cells In Vitro and In Vivo

Medicines ◽  
2018 ◽  
Vol 5 (4) ◽  
pp. 124 ◽  
Author(s):  
Yukako Edo ◽  
Amane Otaki ◽  
Kazuhito Asano
Keyword(s):  
Epithelial Cells ◽  
Nasal Lavage ◽  
Oxygen Species ◽  
Male Mice ◽  
Nasal Epithelial Cells ◽  
Nasal Symptoms ◽  
Human Nasal Epithelial Cells ◽  
Culture Supernatants

Background: Thioredoxin (TRX) acts as both a scavenger of reactive oxygen species (ROS) and an immuno-modulator. Although quercetin has been shown to favorably modify allergic rhinitis (AR) symptoms, its influence on TRX production is not well defined. The present study was designed to examine whether quercetin could favorably modify AR symptoms via the TRX production of nasal epithelial cells in vitro and in vivo. Methods: Human nasal epithelial cells (HNEpCs) were stimulated with H2O2 in the presence of quercetin. TRX levels in 24-h culture supernatants were examined with ELISA. BALB/c male mice were intraperitoneally sensitized to ovalbumin (OVA) and intranasally challenged with OVA every other day, beginning seven days after the final sensitization. The mice were orally administered quercetin once a day for five consecutive days, beginning seven days after the final sensitization. Nasal symptoms were assessed by counting the number of sneezes and nasal rubbing behaviors during a 10-min period immediately after the challenge. TRX levels in nasal lavage fluids obtained 6 h after the challenge were examined by ELISA. Results: Treatment with 1.0 nM quercetin increased H2O2-induced TRX levels. The oral administration of 20.0 mg/kg of quercetin significantly inhibited nasal symptoms after the challenge. The same dose of quercetin significantly increased TRX levels in nasal lavage fluids. Conclusions: Quercetin’s ability to increase TRX production may account, at least in part, for its clinical efficacy toward AR.

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.

Expression and localization of tricellulin in human nasal epithelial cells in vivo and in vitro

2009 ◽  
Vol 42 (4) ◽  
pp. 204-211 ◽  
Author(s):  
Tsuyoshi Ohkuni ◽  
Takashi Kojima ◽  
Noriko Ogasawara ◽  
Tomoyuki Masaki ◽  
Takafumi Ninomiya ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Nasal Epithelial Cells ◽  
Human Nasal Epithelial Cells

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

scholarly journals Primary human nasal epithelial cells: a source of poly (I:C) LMW-induced IL-6 production

2018 ◽  
Vol 8 (1) ◽  
Author(s):  
Mahnaz Ramezanpour ◽  
Harrison Bolt ◽  
Alkis James Psaltis ◽  
Peter-John Wormald ◽  
Sarah Vreugde
Keyword(s):  
Epithelial Cells ◽  
Poly I:C ◽  
Nasal Epithelial Cells ◽  
Human Nasal Epithelial Cells

scholarly journals Elovanoids Counteract Inflammatory Signaling, Autophagy, Endoplasmic Reticulum Stress, and Senescence Gene Programming in Human Nasal Epithelial Cells Exposed to Allergens

Pharmaceutics ◽  
2022 ◽  
Vol 14 (1) ◽  
pp. 113
Author(s):  
Alfredo Resano ◽  
Surjyadipta Bhattacharjee ◽  
Miguel Barajas ◽  
Khanh V. Do ◽  
Roberto Aguado-Jiménez ◽  
...  
Keyword(s):  
Endoplasmic Reticulum ◽  
Epithelial Cells ◽  
Inflammatory Responses ◽  
House Dust Mites ◽  
Poly I:C ◽  
Lipid Mediator ◽  
Omega 3 ◽  
Nasal Epithelial Cells ◽  
Human Nasal Epithelial Cells

To contribute to further understanding the cellular and molecular complexities of inflammatory-immune responses in allergic disorders, we have tested the pro-homeostatic elovanoids (ELV) in human nasal epithelial cells (HNEpC) in culture challenged by several allergens. ELV are novel bioactive lipid mediators synthesized from the omega-3 very-long-chain polyunsaturated fatty acids (VLC-PUFA,n-3). We ask if: (a) several critical signaling events that sustain the integrity of the human nasal epithelium and other organ barriers are perturbed by house dust mites (HDM) and other allergens, and (b) if ELV would participate in beneficially modulating these events. HDM is a prevalent indoor allergen that frequently causes allergic respiratory diseases, including allergic rhinitis and allergic asthma, in HDM-sensitized individuals. Our study used HNEpC as an in vitro model to study the effects of ELV in counteracting HDM sensitization resulting in inflammation, endoplasmic reticulum (ER) stress, autophagy, and senescence. HNEpC were challenged with the following allergy inducers: LPS, poly(I:C), or Dermatophagoides farinae plus Dermatophagoides pteronyssinus extract (HDM) (30 µg/mL), with either phosphate-buffered saline (PBS) (vehicle) or ELVN-34 (500 nM). Results show that ELVN-34 promotes cell viability and reduces cytotoxicity upon HDM sensitization of HNEpC. This lipid mediator remarkably reduces the abundance of pro-inflammatory cytokines and chemokines IL-1β, IL-8, VEGF, IL-6, CXCL1, CCL2, and cell adhesion molecule ICAM1 and restores the levels of the pleiotropic anti-inflammatory IL-10. ELVN-34 also lessens the expression of senescence gene programming as well as of gene transcription engaged in pro-inflammatory responses. Our data also uncovered that HDM triggered the expression of key genes that drive autophagy, unfolded protein response (UPR), and matrix metalloproteinases (MMP). ELVN-34 has been shown to counteract these effects effectively. Together, our data reveal a novel, pro-homeostatic, cell-protective lipid-signaling mechanism in HNEpC as potential therapeutic targets for allergies.

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.

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