scholarly journals Taurine promotes the production of CD4+CD25+FOXP3+ Treg cells through regulating IL-35/STAT1 pathway in a mouse allergic rhinitis model

2021 ◽  
Vol 17 (1) ◽  
Author(s):  
Jing Zhou ◽  
Yi Lu ◽  
Wei Wu ◽  
Yunhai Feng
Keyword(s):  
Allergic Rhinitis ◽  
Nasal Mucosa ◽  
Goblet Cell ◽  
Inflammatory Cytokine ◽  
Neutralizing Antibody ◽  
Treg Cells ◽  
Ar Model ◽  
Cytokine Release ◽  
Cell Content ◽  
Taurine Treatment

Abstract Background Allergic rhinitis (AR) is one of the most widespread immune conditions worldwide. However, common treatments often present with significant side effects or are cost-prohibitive for much of the population. A plethora of treatments have been used for the treatment of AR including antihistamines, steroids, and immune modulators. Among the treatments which have shown potential for efficacy in treating AR with a minimum of side effects but remains understudied is the conditionally essential amino acid taurine. Taurine has been previously shown to reduce AR symptoms. Here, we examine the role of taurine in modulating T regulatory cells, modulating the cytokine response in AR, and restoring healthy nasal mucosa. Methods Blood samples from 20 healthy donors and 20 AR patients were compared for CD4+CD25+FoxP3+ T regulatory (Treg) cell population percentage, cytokine release, and STAT1 signaling with and without taurine treatment or IL-35 neutralization. An OVA-induced AR mouse model was administered vehicle, taurine, or taurine plus an IL-35 neutralizing antibody and assayed for sneezing frequency, inflammatory cytokine response, nasal mucosa goblet cell density, and T regulatory cell percentage. CD4+ cells were further examined for cytokine release, STAT1 phosphorylation, and response to an anti-IL-35 antibody with and without a STAT1 inhibitor. Results Comparison of blood from normal donors and AR patients showed a reduction in CD4+CD25+FoxP3+ Treg cells in AR patients and a strong correlation between Treg percentage and IL-35 release. A similar pattern of Treg suppression was found in untreated AR mice when compared to normal control mice wherein there was a reduction in Treg percentage and a corresponding decrease in IL-35 release. AR mice also demonstrated increased sneezing frequency, an infiltration of goblet cell in nasal mucosa, and a reduction in IL-35 release from CD4+ cells. Conversely, IL-4, IL-5, and IL-13 secretion from CD4+ cells were increased in AR model mice, as was STAT1 phosphorylation. When AR mice were treated with taurine, sneezing frequency and nasal mucosa goblet cell content were reduced while Treg abundance was increased to that of normal mice. Accordingly, IL-35 release was restored, while IL-4, IL-5, and IL-13 secretion from CD4+ cells were suppressed. Likewise, STAT1 phosphorylation was inhibited with taurine treatment. Taurine-treated mice also given an IL-35 neutralizing antibody exhibited AR pathology including frequent sneezing and high nasal goblet cell content while retaining a restoration of Tregs. Furthermore, murine AR model CD4+ cells exposed to recombinant IL-35 responded with a reduction in inflammatory cytokine release and a decrease in STAT1 phosphorylation, mimicking the effect of taurine treatment. Conclusions Taurine induces release of IL-35 in AR; IL-35 promotes the production of CD4+CD25+FoxP3+ Treg cells via a STAT1-dependent pathway. The restoration of Treg populations by taurine normalizes the inflammatory response, reduces AR symptomology, and reduces histopathologic signs of AR.

scholarly journals Taurine Promotes the Production of CD4+CD25+FOXP3+ Treg Cells through Regulating IL-35/STAT1 Pathway in a Mouse Allergic Rhinitis Model

2020 ◽  
Author(s):  
Jing Zhou ◽  
Yi Lu ◽  
Wei Wu ◽  
Yunhai Feng
Keyword(s):  
Allergic Rhinitis ◽  
Nasal Mucosa ◽  
Goblet Cell ◽  
Inflammatory Cytokine ◽  
Neutralizing Antibody ◽  
Treg Cells ◽  
Ar Model ◽  
Cytokine Release ◽  
Cell Content ◽  
Taurine Treatment

Abstract Background: Allergic rhinitis (AR) is one of the most widespread immune conditions worldwide. However, common treatments often present with significant side effects or are cost-prohibitive for much of the population. A plethora of treatments have been used for the treatment of AR including antihistamines, steroids, and immune modulators. Among the treatments which have shown potential for efficacy in treating AR with a minimum of side effects but remains understudied is the conditionally essential amino acid taurine. Taurine has been previously shown to reduce AR symptoms. Here, we examine the role of taurine in modulating T regulatory cells, modulating the cytokine response in AR, and restoring healthy nasal mucosa.Methods: Blood samples from 20 healthy donors and 20 AR patients were compared for CD4+CD25+FoxP3+ T regulatory (Treg) cell population percentage, cytokine release, and STAT1 signaling with and without taurine treatment or IL-35 neutralization. An OVA-induced AR mouse model was administered vehicle, taurine, or taurine plus an IL-35 neutralizing antibody and assayed for sneezing frequency, inflammatory cytokine response, nasal mucosa goblet cell density, and T regulatory cell percentage. CD4+ cells were further examined for cytokine release, STAT1 phosphorylation, and response to an anti-IL-35 antibody with and without a STAT1 inhibitor. Results: Comparison of blood from normal donors and AR patients showed a reduction in CD4+CD25+FoxP3+ Treg cells in AR patients and a strong correlation between Treg percentage and IL-35 release. A similar pattern of Treg suppression was found in untreated AR mice when compared to normal control mice wherein there was a reduction in Treg percentage and a corresponding decrease in IL-35 release. AR mice also demonstrated increased sneezing frequency, an infiltration of goblet cell in nasal mucosa, and a reduction in IL-35 release from CD4+ cells. Conversely, IL-4, IL-5, and IL-13 secretion from CD4+ cells were increased in AR model mice, as was STAT1 phosphorylation. When AR mice were treated with taurine, sneezing frequency and nasal mucosa goblet cell content were reduced while Treg abundance was increased to that of normal mice. Accordingly, IL-35 release was restored, while IL-4, IL-5, and IL-13 secretion from CD4+ cells were suppressed. Likewise, STAT1 phosphorylation was inhibited with taurine treatment. Taurine-treated mice also given an IL-35 neutralizing antibody exhibited AR pathology including frequent sneezing and high nasal goblet cell content while retaining a restoration of Tregs. Furthermore, murine AR model CD4+ cells exposed to recombinant IL-35 responded with a reduction in inflammatory cytokine release and a decrease in STAT1 phosphorylation, mimicking the effect of taurine treatment. Conclusions: Taurine induces release of IL-35 in AR; IL-35 promotes the production of CD4+CD25+FoxP3+ Treg cells via a STAT1-dependent pathway. The restoration of Treg populations by taurine normalizes the inflammatory response, reduces AR symptomology, and reduces histopathologic signs of AR.

scholarly journals The extract of black cumin, licorice, anise, and black tea alleviates OVA-induced allergic rhinitis in mouse via balancing activity of helper T cells in lung

2021 ◽  
Vol 17 (1) ◽  
Author(s):  
Chengsong Liao ◽  
Yangyang Han ◽  
Zhijing Chen ◽  
Huricha Baigude
Keyword(s):  
Allergic Rhinitis ◽  
Nasal Mucosa ◽  
Aqueous Extract ◽  
Nigella Sativa ◽  
Inflammatory Cells ◽  
Serum Levels ◽  
Lavage Fluid ◽  
Ar Model ◽  
Control Group ◽  
Black Cumin

Abstract Background A formulation of black cumin (Nigella sativa L.), licorice (Glycyrrhiza glabra L.), anise (Pimpinella anisum L.) and tea (Camellia sinensis (L.) Kuntze) (denoted BLAB tea) is traditionally used to relief allergy reaction including allergic rhinitis. However, little is known about its underlining mechanism of anti-allergic effects. Methods To investigate the anti-allergenic mechanism of BLAB tea, we treated ovalbumin (OVA)-induced allergic rhinitis (AR) model of mice with BLAB tea, and elucidated its possible mechanism of action. Mice in the control group were treated with phosphate-buffered saline only. Subsequently, the infiltration of different inflammatory cells was measured. In addition, histopathological changes in the nasal mucosa, and the levels of allergen-specific cytokines and OVA-specific immunoglobulins were measured. Results The aqueous extract of BLAB significantly alleviated the nasal symptoms and reduced the accumulation of inflammatory cells in the nasal mucosa and nasal lavage fluid of AR model of mice. Conclusion The aqueous extract of BLAB induced the production of Th1 and Treg cytokines and inhibited the release of Th2 cytokines and histamine in nasal mucosa and serum of mice while decreasing the serum levels of OVA-specific IgE, IgG1, and IgG2a. These results suggest the potential of the aqueous extract of BLAB as a treatment option for allergic diseases.

scholarly journals D-Pinitol Attenuated Ovalbumin-induced Allergic Rhinitis in Experimental Mice Via Balancing Th1/Th2 Response

2021 ◽  
Author(s):  
Xiying You ◽  
Xiaopeng Sun ◽  
Junfei Kong ◽  
Jifeng Tian ◽  
Yanping Shi ◽  
...  
Keyword(s):  
Allergic Rhinitis ◽  
Immune Responses ◽  
Nasal Mucosa ◽  
Potential Effect ◽  
Ar Model ◽  
Cytokine Signaling ◽  
Control Group ◽  
Th2 Response ◽  
T Box ◽  
Th1 Immune Responses

Allergic rhinitis (AR) is a complex, chronic immunoinflammatory disorder of the membrane lining of the nasal mucosa. D-Pinitol is considered a cyclic polyol with a potential effect against various allergies. In the present study, we evaluated the anti-allergic effect of pinitol on ovalbumin (OVA)-induced AR model in mice. BALB/c mice were initially sensitized with an intraperitoneal injection of OVA and divided into 5 groups (n=18, in each group) for a treating schedule of distilled water (DW), montelukast (10 mg/kg), and pinitol (5, 10, and 20 mg/kg) through the mouth. Two saline-injected groups were considered as controls by orally administrating DW and pinitol 20. Thereafter, test and control groups were intranasally challenged by OVA and saline, respectively. Our results showed that the OVA challenge caused a marked elevation in AR symptoms like nasal rubbing, sneezing, and discharge which were remarkably diminished using pinitol (10 and 20 mg/kg) and the results were comparable with montelukast. Additionally, increased levels of total and OVA-specific serum Immunoglobulin (Ig) E and IgG1 were significantly attenuated by pinitol as compared to the control group but not the montelukast group. In AR-induced mice, pinitol had significant modulatory effects on representative markers of Th2 (GATA binding protein 3), signal transducer and activator of transcription-6, Interleukins (IL)-4, IL-5, IL-13, suppressors of cytokine signaling 1, Toll-like receptor 4, and myeloid differentiation factor 88), and Type 1 T helper (Th1) immune responses (T-box protein expressed in T cells and Interferon-gamma) as well as the histopathological aberrations induced in the nasal mucosa. In conclusion, Pinitol had potential effects on OVA-induced AR mice through amelioration of nasal symptoms and balancing the Th1/Th2 immune responses during the allergic rhinitis condition.

scholarly journals Anti-Interleukin-1 Beta/Tumor Necrosis Factor-Alpha IgY Antibodies Reduce Pathological Allergic Responses in Guinea Pigs with Allergic Rhinitis

2016 ◽  
Vol 2016 ◽  
pp. 1-11 ◽  
Author(s):  
Hu Wei-xu ◽  
Zhou Wen-yun ◽  
Zhu Xi-ling ◽  
Wen Zhu ◽  
Wu Li-hua ◽  
...  
Keyword(s):  
Allergic Rhinitis ◽  
Treatment Group ◽  
Nasal Mucosa ◽  
Guinea Pigs ◽  
Interleukin 1 ◽  
Allergic Inflammation ◽  
Inflammatory Cells ◽  
Lavage Fluid ◽  
Ar Model ◽  
Necrosis Factor Alpha

This study aims to determine whether the combined blockade of IL-1βand TNF-αcan alleviate the pathological allergic inflammatory reaction in the nasal mucosa and lung tissues in allergic rhinitis (AR) guinea pigs. Healthy guinea pigs treated with saline were used as the healthy controls. The AR guinea pigs were randomly divided into (1) the AR model group treated with intranasal saline; (2) the 0.1% nonspecific IgY treatment group; (3) the 0.1% anti-TNF-αIgY treatment group; (4) the 0.1% anti-IL-1βIgY treatment group; (5) the 0.1% combined anti-IL-1βand TNF-αIgY treatment group; and (6) the fluticasone propionate treatment group. The inflammatory cells were evaluated using Wright’s staining. Histopathology was examined using hematoxylin-eosin staining. The results showed that the number of eosinophils was significantly decreased in the peripheral blood, nasal lavage fluid, and bronchoalveolar lavage fluid (P<0.05), and eosinophil, neutrophil, and lymphocyte infiltration and edema were significantly reduced or absent in the nasal mucosa and lung tissues (P<0.05) in the combined 0.1% anti-IL-1β- and TNF-αIgY-treated guinea pigs. The data suggest that topical blockade of IL-1βand TNF-αcould reduce pathological allergic inflammation in the nasal mucosa and lung tissues in AR guinea pigs.

Effect of PM2.5 on MicroRNA Expression and Function in Nasal Mucosa of Rats With Allergic Rhinitis

2020 ◽  
Vol 34 (4) ◽  
pp. 543-553
Author(s):  
Yu Huang ◽  
Zhi-Qiang Guo ◽  
Ru-Xin Zhang ◽  
Ren-Wu Zhao ◽  
Wei-Yang Dong ◽  
...  
Keyword(s):  
Allergic Rhinitis ◽  
Nasal Mucosa ◽  
Mirna Expression ◽  
Expression Profiles ◽  
Mirna Gene ◽  
Ar Model ◽  
Qrt Pcr ◽  
Mirna Expression Profiles ◽  
Differentially Expressed Mirnas ◽  
And Function

Background Particulate matter 2.5 (PM2.5) refers to particulate matter with aerodynamic equivalent diameter less than or equal to 2.5 µm, which is an important component of air pollution. PM2.5 aggravates allergic rhinitis (AR) and promotes AR nasal mucosa inflammation. Therefore, the influence of PM2.5 inhalation exposure on microRNA (miRNA) expression profiles and function in the nasal mucosa of AR rats was investigated. Methods Female Sprague Dawley rats were distributed randomly to 2 groups: AR model PM2.5 exposure group (ARE group) and AR model PM2.5-unexposed control group (ARC group). The rats of ARE group were made to inhale PM2.5 at a concentration of 200 µg/m3, 3 h/day, for 30 days. miRNA expression profiles of the nasal mucosa from both groups were determined using an miRNA gene chip and were verified by quantitative real-time PCR (qRT-PCR). Gene function enrichment analysis was performed using bioinformatics analysis. Results The ARE group revealed 20 significantly differentially expressed miRNAs, including 4 upregulated and 16 downregulated miRNAs (fold change > 1.5 or < 0.66, P < .05). Of these, 9 selected miRNAs were verified by qRT-PCR, and the results of 8 miRNAs were in accordance with the miRNA gene chip results, with highly positive correlation ( r = .8583, P = .0031). Numerous target genes of differentially expressed miRNAs were functionally enriched in high-affinity immunoglobulin E receptor signaling, ErbB signaling, mucin O-glycans biosynthesis, transforming growth factor β signaling, mitogen-activated protein kinase signal transduction, phosphatidylinositol signaling, mucopolysaccharide biosynthesis, mammalian target of rapamycin signaling, T cell receptor signaling, Wnt signaling, chemokine signal transduction, and natural killer cell-mediated cytotoxicity pathways. Conclusions PM2.5 causes significant changes in miRNA expression in the nasal mucosa of AR rats. miRNA plays an important role in regulating PM2.5 effects in AR rat biological behavior and mucosal inflammation. This study provides a theoretical basis for the prevention and treatment of AR from the effects of environmental pollution on the gene regulation mechanism.

scholarly journals MicroRNA-29 mediates anti-inflammatory effects and alleviation of allergic responses and symptoms in mice with allergic rhinitis

2021 ◽  
Vol 17 (1) ◽  
Author(s):  
Jia Wang ◽  
Jinshu Yin ◽  
Hong Peng ◽  
Aizhu Liu
Keyword(s):  
Allergic Rhinitis ◽  
Nasal Mucosa ◽  
Immunoglobulin E ◽  
Underlying Mechanism ◽  
Lavage Fluid ◽  
Specific Ige ◽  
Ar Model ◽  
Protein Levels ◽  
Mucosa Cell

Abstract Background To investigate the role of microRNA-29 (miR-29) in mice with allergic rhinitis (AR) and its underlying mechanism. Methods AR model was established in BALB/c mice by intraperitoneal sensitization and intranasal challenge with ovalbumin (OVA). miRNA expression was examined in the nasal mucosa tissues of mice and patients with AR, and miRNA-29 was found to be downregulated. To unveil the role of miRNA-29 in AR, it was overexpressed in the nasal mucosa of AR mice by intranasal administration of miRNA-29 agomir. The symptoms of nasal rubbing and sneezing were recorded and evaluated. miR-29 expression, OVA-specific immunoglobulin E (IgE) concentration, pro-inflammatory cytokines levels, eosinophils number, and cleaved caspase-3 and CD276 expression were examined in nasal mucosa tissues and nasal lavage fluid (NALF) by qRT-PCR, ELISA, hematoxylin and eosin staining, western blotting, or immunohistochemistry, respectively. TUNEL assay was used to analyze nasal mucosa cells apoptosis. Results Decreased expression of miR-29 was observed in AR, the symptoms of which were alleviated by overexpressing miR-29. In addition, overexpression of miR-29 markedly reduced the concentration of OVA-specific IgE, the levels of IL-4, IL-6, IL-10, and IFN-γ, the pathological alterations and eosinophils infiltration in the nasal mucosa. Furthermore, restoration of miR-29 expression reduced nasal mucosa cell apoptosis. Moreover, overexpression of miR-29 significantly attenuated CD276 mRNA and protein levels in nasal mucosa cells. Conclusion MiR-29 mediated antiallergic effects in OVA-induced AR mice by decreasing inflammatory response, probably through targeting CD276. MiRNA-29 may serve as a potential novel therapeutic target for the treatment of AR.

Effects of Ursolic Acid on the Expression of Th1–Th2-related Cytokines in a Rat Model of Allergic Rhinitis After PM2.5 Exposure

2020 ◽  
Vol 34 (5) ◽  
pp. 587-596 ◽  
Author(s):  
Na Sun ◽  
Zhijin Han ◽  
Hong Wang ◽  
Zhiqiang Guo ◽  
Congrui Deng ◽  
...  
Keyword(s):  
Allergic Rhinitis ◽  
Particulate Matter ◽  
Ursolic Acid ◽  
Nasal Mucosa ◽  
Rat Model ◽  
Ar Model ◽  
Eosinophilic Infiltration ◽  
Th2 Cytokines ◽  
Nasal Symptoms ◽  
Pm2.5 Exposure

Background Allergic rhinitis (AR) is a global health problem and closely related to environmental factors. Ursolic acid (UA) has potential in the treatment of allergic inflammation. The effects of UA intervention on PM2.5-induced AR remain uncertain. Objective To assess the effects of UA on nasal symptoms and the expression of T-helper (Th)1–Th2-related cytokines in a rat model of AR after fine particulate matter (particulate matter ≤ 2.5 µm [PM2.5]) exposure. Methods A total of 40 healthy female Sprague-Dawley rats were randomly divided into 4 groups: normal control group (NC group), ovalbumin (OVA)- induced AR model (AR group), PM2.5-exposed AR group exposed to 200 g/m3 PM2.5 for 30 days via inhalation (ARE group), and a group with UA intervention to the AR model after PM2.5 exposure (UA group). UA intervention was adopted after PM2.5 exposure in the UA group. Nasal symptoms and levels of Th1–Th2 cytokines in the serum were detected in each individual rat. The pathological changes and expression of Eotaxin in the nasal mucosa of each individual rat were examined by histology. Results PM2.5 significantly increased the number of sneezes and nasal rubs in the rats with AR, and UA alleviated these symptoms. UA decreased interleukin (IL)-4, IL-5, IL-13, Eotaxin-1, and OVA Immunoglobulin E (IgE) protein levels. In the AR group, hematoxylin and eosin staining showed disordered arrangement of the nasal mucosa epithelium, cell shedding, eosinophilic infiltration, swelling of the glands, and submucosal vascular congestion. UA group showed reduced eosinophilic infiltration and orderly arrangement of the mucosal epithelium when compared with the ARE group. Immunohistochemical results showed that the expression of Eotaxin in the UA group was lower than that in the ARE group. Conclusion UA could relieve nasal symptoms caused by PM2.5 exposure, the possible mechanism of which is to inhibit the expression of Th2 cytokines, eosinophilic infiltration, and specific IgE production.

scholarly journals PM2.5 Exacerbates Oxidative Stress and Inflammatory Response through the Nrf2/NF-κB Signaling Pathway in OVA-Induced Allergic Rhinitis Mouse Model

2021 ◽  
Vol 22 (15) ◽  
pp. 8173
Author(s):  
Chun Hua Piao ◽  
Yanjing Fan ◽  
Thi Van Nguyen ◽  
Hee Soon Shin ◽  
Hyoung Tae Kim ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Allergic Rhinitis ◽  
Inflammatory Response ◽  
Mouse Model ◽  
Signaling Pathway ◽  
Nasal Mucosa ◽  
Inflammatory Cytokine ◽  
Allergic Airway Inflammation ◽  
Nrf2 Signaling Pathway ◽  
Pm2.5 Exposure

Air pollution-related particulate matter (PM) exposure reportedly enhances allergic airway inflammation. Some studies have shown an association between PM exposure and a risk for allergic rhinitis (AR). However, the effect of PM for AR is not fully understood. An AR mouse model was developed by intranasal administration of 100 μg/mouse PM with a less than or equal to 2.5 μm in aerodynamic diameter (PM2.5) solution, and then by intraperitoneal injection of ovalbumin (OVA) with alum and intranasal challenging with 10 mg/mL OVA. The effects of PM2.5 on oxidative stress and inflammatory response via the Nrf2/NF-κB signaling pathway in mice with or without AR indicating by histological, serum, and protein analyses were examined. PM2.5 administration enhanced allergic inflammatory cell expression in the nasal mucosa through increasing the expression of inflammatory cytokine and reducing the release of Treg cytokine in OVA-induced AR mice, although PM2.5 exposure itself induced neither allergic responses nor damage to nasal and lung tissues. Notably, repeated OVA-immunization markedly impaired the nasal mucosa in the septum region. Moreover, AR with PM2.5 exposure reinforced this impairment in OVA-induced AR mice. Long-term PM2.5 exposure strengthened allergic reactions by inducing the oxidative through malondialdehyde production. The present study also provided evidence, for the first time, that activity of the Nrf2 signaling pathway is inhibited in PM2.5 exposed AR mice. Furthermore, PM2.5 exposure increased the histopathological changes of nasal and lung tissues and related the inflammatory cytokine, and clearly enhanced PM2.5 phagocytosis by alveolar macrophages via activating the NF-κB signaling pathway. These obtained results suggest that AR patients may experience exacerbation of allergic responses in areas with prolonged PM2.5 exposure.

scholarly journals MicroRNA-133b Ameliorates Allergic Inflammation and Symptom in Murine Model of Allergic Rhinitis by Targeting Nlrp3

2017 ◽  
Vol 42 (3) ◽  
pp. 901-912 ◽  
Author(s):  
Lifeng Xiao ◽  
Li Jiang ◽  
Qi Hu ◽  
Yuru Li
Keyword(s):  
Allergic Rhinitis ◽  
Nasal Mucosa ◽  
Nlrp3 Inflammasome ◽  
Immunoglobulin E ◽  
Ar Model ◽  
Allergic Symptom ◽  
Inflammasome Activation ◽  
Nlrp3 Inflammasome Activation ◽  
Tnf Α ◽  
Ifn Γ

Background: Emerging evidences indicate that post-transcriptional regulation by microRNAs is critical in allergic rhinitis (AR) pathogenesis. MircroRNA-133b (miR-133b) was recently suggested as a potential predictor of AR. However, the in vivo effect of miR-133b on AR is unclear. Methods: AR model was established in BALB/c mice by intraperitoneal sensitization and intranasal challenge with ovalbumin (OVA). MiR-133b agomir was then intranasally administrated to mice after OVA challenge for another 7 days. The symptom of nasal rubbing and sneezing were recorded after the last OVA challenge. Nasal mucosa tissues and serum were collected. MiR-133b expression, serum OVA-specific immunoglobulin E (IgE) concentration, proinflammatory cytokines (TNF-α, IL-4, IL-5, IL-10 and IFN-γ) levels, and Nlrp3 inflammasome activation were measured by RT-PCR, ELISA, western blotting or immunohistochemistry, respectively. Histopathologic changes were evaluated using hematoxylin and eosin and Sirius red staining. The luciferase activity and protein expression of Nlrp3 were also determined. Results: MiR-133b expression was significantly decreased in nasal mucosa of AR mice, which was restored by nasal administration with miR-133b agomir. Upregulation of miR-133b markedly reduced the concentration of OVA-specific IgE, the frequencies of nasal rubbing and sneezing, and the levels of cytokines (TNF-α, IL-4, IL-5 and IFN-γ). Levels of IL-4, IL-5, IL-10 and IFN-γ produced by cervical lymph node cells were significantly lowered in miR-133b agomir-treated mice. Moreover, miR-133b also appeared to strongly attenuate pathological alterations and eosinophils and mast cells infiltration in nasal mucosa. Notably, we demonstrated for the first time that miR-133b negatively regulated Nlrp3 expression through binding with the 3’ untranslated region of Nlrp3. Consequently, infection of miR-133b in nasal mucosa remarkably suppressed the Nlrp3 inflammasome activation, as evidenced by reduced Nlrp3, Caspase-1, ASC, IL-18 and IL-1 expressions. Conclusion: MiR-133b alleviates allergic symptom in AR mice by inhibition of Nlrp3 inflammasome-meditated inflammation. These findings provide us an insight into the potential role of miR-133b in relation to AR treatment.

scholarly journals Is resveratrol therapeutic when used to treat allergic rhinitis in rats?

2016 ◽  
Vol 39 (2) ◽  
pp. 63 ◽  
Author(s):  
Kazım Bozdemir ◽  
Ethem Şahin ◽  
Niyazi Altintoprak ◽  
Nuray B Muluk ◽  
Betül P Cengiz ◽  
...  
Keyword(s):  
Allergic Rhinitis ◽  
Mast Cell ◽  
Lamina Propria ◽  
Nasal Mucosa ◽  
Goblet Cell ◽  
Cell Infiltration ◽  
Cell Numbers ◽  
Resveratrol Treatment ◽  
Vascular Congestion ◽  
And Control

Purpose: Resveratrol has anti-infective, anti-inflammatory and antioxidant activities. The purpose of this study was to determine the effect of resveratrol in a rat experimental model of allergic rhinitis (AR). Methods: Wistar albino rats were divided into three groups: control (n=7), AR with no treatment (AR+NoTr, n=7) and AR with resveratrol treatment (AR+Res, n=7). For AR+Res, AR was induced and resveratrol given on days 21-28. On day 28, the total blood IgE levels were measured. Allergic symptoms (sneezing, nose-rubbing, eye lacrimation and nasal congestion) were scored on a 0-3 point scale, and histopathological changes in the nasal mucosa were evaluated. Results: Allergic symptom score of AR+NoTr was higher than the other two groups and the score of AR+Res was higher than the control group. Histopathologically, neither ciliary loss nor chondrocyte hypertrophy differed among the three groups; however, vascular congestion, inflammatory and plasma cell numbers, eosinophil and mast cell infiltration and goblet cell numbers were higher and mast cell infiltration was more prominent in AR+NoTr than in AR+Res and control. AR+Res and control did not differ significantly in any histological parameter. In AR+NoTr, nasal mucosa exhibited ciliary loss, squamous epithelial metaplasia, inflammatory cell infiltration, vascular congestion of the lamina propria and goblet cell epithelial metaplasia. In AR+Res, goblet cell metaplasia was focal or absent and infiltration of the lamina propria by inflammatory cells, eosinophils, and plasma cells was reduced relative to AR+NoTr. Conclusion: Allergic symptoms and tissue reactions were reduced by resveratrol treatment in rats with experimentally-induced AR.

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