Animal Model Of Allergic Rhinitis Research Articles

MiR-224-5p Attenuates Allergic Responses in Mice with Allergic Rhinitis by Modulating the Th1/Th2 Response.

Allergic rhinitis (AR) is a common chronic respiratory disease that has become a global health problem. miRNAs play an important role in multiple immune and inflammatory diseases, including AR. In this work, the mechanism by which miR-224-5p regulates AR in vivo and in vitro was examined. Human nasal epithelial cells (HNEpCs) were used to establish an AR cell model induced by Der P1, and C57BL/6 mice were used to establish an AR animal model induced by OVA (ovalbumin). RT-qPCR was used to determine the level of miR-224-5p; western blot analysis was used to determine GATA3; ELISA was used to determine the levels of OVA-specific IgE, IFN-γ, IL-4, IL-5, and IL-13; flow cytometry was used to determine the differentiation of Th1 and Th2 cells; and HE and PAS staining was used to observe the histopathological alterations in the mouse nasal mucosa and spleen. miR-224-5p was downregulated in nasal mucosa from mice with AR and an AR cell model. Overexpressed miR-224-5p can improve AR development and attenuate AR symptoms by regulating GATA3-mediated Th1/Th2 responses. miR-224-5p attenuates allergic reactions in mice with AR by regulating the Th1/Th2 response.

Regulation of T Helper Cell Type 2 Immune Response by Controlling Beta-2 Adrenergic Receptor in Dendritic Cells of Patients with Allergic Rhinitis

Introduction: Allergic diseases are mediated by T helper cell type 2 (Th2) cells, which are differentiated by dendritic cells (DCs). Recently, it was reported that cAMP concentration in DCs is important for inducing allergic responses. However, the regulatory function of cAMP in DCs in Th2 immune responses is unclear. It was hypothesized that the regulation of G protein-coupled receptors (GPCRs) to increase cAMP levels in DCs would reduce Th2 immune responses. Methods: Human DCs from patients with allergic rhinitis (AR) and from healthy controls were subjected to next-generation sequencing (NGS) to identify potential GPCR. To investigate the functions of GPCR agonists, the in vitro co-culture experiment that THP-1 cells were differentiated into DCs and cultured with human CD4+ T-cells and an AR animal in vivo model were used. Results: Among the GPCRs, the beta-2 adrenergic receptor (ADRB2) of allergic DCs was significantly increased by NGS analysis. The expression of ADRB2 was also increased in Der p 1-treated DCs, which was reduced by treatment with the ADRB2 agonist salbutamol. Salbutamol treatment induced cAMP production in THP-1 derived DCs. In an in vitro co-culture experiment, salbutamol-treated DCs reduced the secretion of Th2 cytokine. In an in vivo AR animal experiment, salbutamol-administered mice showed reduced allergic behavior and Th2 cytokine expression in the nasal mucosa. Conclusions: The regulation of ADRB2 with salbutamol alleviated the allergic response in vitro DC-T cell co-culture and in vivo AR animal models, suggesting that ADRB2 is a therapeutic target for AR and that ADRB2 agonists may be a promising medication for AR.

Mesenchymal stem cell derived extracellular vesicles loaded thermosensitive chitosan-based hydrogel alleviates allergic rhinitis in mouse model

Allergic rhinitis (AR) has gained an increasing prevalence over the years, a more effective and safe treatment strategy need to be carried out. Mesenchymal stem cell derived extracellular vesicles (MSC-EVs) show great therapeutic potential for AR, however, their low bioavailability through currently available delivery methods inhibits the process of clinical application. In the present study, an injectable thermosensitive chitosan based hydrogel was developed as an intranasal delivery platform for bone marrow-derived MSC-EVs (BMSC-EVs) and BMSC-EVs were proved to be effective in treating AR animal models for the first time. Our results showed that the BMSC-EVs loaded thermosensitive chitosan based hydrogel (BMSC-EVs@CHI hydrogel) could be prepared easily by ion-crosslinking and its gelation properties were suitable for intranasal administration. In vitro studies demonstrated that the BMSC-EVs@CHI hydrogel could achieve sustained release of BMSC-EVs mainly by degradation control and preserve the therapeutic functions of BMSC-EVs. An in vivo experiment revealed that the BMSC-EVs@CHI hydrogel could enhance the efficacy of BMSC-EVs for AR alleviation. This study provides a suitable delivery platform for BMSC-EVs-based AR therapy.

Effects of 101BHG-D01, a novel M receptor antagonism, on allergic rhinitis in animal models and its mechanism

Allergic rhinitis (AR) is a nasal mucosal disease with sneezing and nasal itching as the main symptoms. Although AR treatment continues to improve, there remains a lack of effective drugs. There are still controversies regarding whether anticholinergic drugs can effectively and safely relieve the symptoms of AR and reduce inflammation in the nasal mucosa. Here, we synthesized 101BHG-D01, which is a novel anticholinergic drug that mainly targets the M3 receptor and may reduce the adverse effects of other anticholinergic drugs on the heart. We evaluated the effects of 101BHG-D01 on AR and investigated the potential molecular mechanism of anticholinergic therapy for AR. We found that 101BHG-D01 effectively alleviated AR symptoms, reduced the infiltration of inflammatory cells and attenuated the expression of inflammatory factors (IL-4, IL-5, IL-13, etc.) in various AR animal models. In addition, 101BHG-D01 reduced the activation of mast cells and the release of histamine from rat peritoneal mesothelial cells (RPMCs) challenged by IgE. Moreover, 101BHG-D01 reduced the expression of MUC5AC in IL-13-challenged rat nasal epithelial cells (RNECs) and human nasal epithelial cells (HNEpCs). Furthermore, IL-13 stimulation significantly increased JAK1 and STAT6 phosphorylation, which was suppressed by 101BHG-D01. We demonstrated that 101BHG-D01 reduced mucus secretion and inflammatory cell infiltration in the nasal mucosa, which may occur through a reduction in activation of the JAK1-STAT6 signaling pathway, indicating that 101BHG-D01 is a potent and safe anticholinergic therapy for AR.

CircARF3 Mitigates Allergic Rhinitis through Targeting microRNA-205-5p/Sirtuin 5 Axis

Introduction: Circular RNAs (circRNAs) are essential in the progression of allergic rhinitis (AR). The purpose of this research was to examine the role of circRNA ADP-ribosylation factor 3 (circARF3) in the pathogenesis of AR. Methods: To generate an animal model of AR, mice were treated with house dust mite (HDM), and mice nasal epithelial cells (NEpCs) were treated with IL-4/IL-13 to imitate the inflammatory damage of AR in vitro. Sanger sequencing, qRT-PCR, and RNAse R digestion assays all validated the circularization structure of circARF3. The levels of circARF3, miR-205-5p, and sirtuin 5 (SIRT5) were determined by qRT-PCR or Western blotting. Luciferase reporter, RNA immunoprecipitation, and pull-down experiments were used to investigate the regulatory network. Flow cytometry was used to investigate the rate of cell apoptosis, and Western blotting was used to determine the levels of apoptotic-related proteins (cleaved caspase 3, cleaved polyadenosine-diphosphate-ribose polymerase) and HMGB1, TLR4, and MyD88. Enzyme-linked immunosorbent assay was used to assess the inflammatory response. Hematoxylin-eosin staining and TUNEL were used to detect the histology of injury and apoptosis of nasal mucosa tissues. Results: CircARF3 and SIRT5 levels were reduced in HDM-treated animals and IL-4/IL-13-treated NEpCs, while miR-205-5p expression was increased. CircARF3 was generated by back-splicing exons 3–5 with a stable circular shape. CircARF3 overexpression mitigated IL-4/IL-13-induced apoptosis in NEpCs by inhibiting miR-205-5p. SIRT5 upregulation attenuated IL-4/IL-13-induced inflammatory injury in NEpCs, and SIRT5 knockdown induced opposite effects. miR-205-5p silencing reversed the effects of SIRT5 knockdown on IL-4/IL-13-induced inflammatory injury. Furthermore, circARF3 overexpression alleviated histological abnormalities, apoptosis, inflammatory response, and HMGB1/TLR4 signaling activation in HDM-treated animals. Conclusion: CircARF3 inhibited cell apoptosis and inflammation via the miR-205-5p/SIRT5 axis in IL-4/IL-13-treated NEpCs and HDM-treated mice.

MIR222HG attenuates macrophage M2 polarization and allergic inflammation in allergic rhinitis by targeting the miR146a-5p/TRAF6/NF-κB axis.

Although M2 macrophages are involved in the orchestration of type 2 inflammation in allergic diseases, the mechanisms underlying non-coding RNA (ncRNA)-mediated macrophage polarization in allergic rhinitis (AR) have not been systematically understood. Here, we identified long non-coding RNA (lncRNA) MIR222HG as a key regulator of macrophage polarization and revealed its role in AR. Consistent with our bioinformatic analysis of GSE165934 dataset derived from the Gene Expression Omnibus (GEO) database, lncRNA-MIR222HG and murine mir222hg were downregulated in our clinical samples and animal models of AR, respectively. Mir222hg was upregulated in M1 macrophages and downregulated in M2 macrophages. The allergen-ovalbumin facilitated polarization of RAW264.7 cells to the M2 phenotype, accompanied by the downregulation of mir222hg expression in a dose-dependent manner. Mir222hg facilitates macrophage M1 polarization and reverses M2 polarization caused by ovalbumin. Furthermore, mir222hg attenuates macrophage M2 polarization and allergic inflammation in the AR mouse model. Mechanistically, a series of gain- and loss-of-function experiments and rescue experiments were performed to verify the role of mir222hg as a ceRNA sponge that adsorbed miR146a-5p, upregulated Traf6, and activated the IKK/IκB/P65 pathway. Collectively, the data highlight the remarkable role of MIR222HG in the modulation of macrophage polarization and allergic inflammation, as well as its potential role as a novel AR biomarker or therapeutic target.

Immunomodulatory properties of mesenchymal stem cells: A potential therapeutic strategy for allergic rhinitis.

Allergic rhinitis is a highly prevalent chronic inflammatory disorder of the nasal mucosa that poses a significant burden on patients' health and quality of life. Current therapies for allergic rhinitis are unable to reinstate immune homeostasis or are restricted by specific allergens. Potential therapeutic strategies for allergic rhinitis are urgently needed. Mesenchymal stem cells (MSCs) are immune-privileged, have strong immunomodulatory effects, and can be easily isolated from various sources. Thus, MSC-based therapies demonstrate potential for treating inflammatory diseases. Recently, numerous studies have investigated the therapeutic effects of MSCs in animal models of allergic rhinitis. Here, we review the immunomodulatory effects and mechanisms of MSCs on allergic airway inflammation, especially allergic rhinitis, highlight the recent research regarding MSCs in the modulation of immune cells, and discuss the clinical potential of MSC-based therapy for allergic rhinitis.

Experimental observation of the effect of immunotherapy on CD4+ T cells and Th1/Th2 cytokines in mice with allergic rhinitis

The present study aims to investigate the effect of immunotherapy in a mouse model of allergic rhinitis (AR) and to explore the possible molecular mechanisms of action. An animal model of AR was established by sensitization and challenge of BALB/c mice with house dust mite (HDM) extract. The mice were injected subcutaneously with HDM for immunotherapy. AR nasal symptoms were evaluated according to the frequencies of nose rubbing and sneezing and the degree of rhinorrhea. The nasal mucosa and lung tissue architecture and inflammatory status by histological analysis; the infiltration of eosinophils in nasal lavage fluid (NALF) of mice was observed by Diff-Quik stain; ELISA-based quantification of serum HDM-specific IgE and TH1/TH2 cytokine concentration; and flow cytometry detected the number of serum CD4+/CD8+ cells to evaluate the mechanism of immunotherapy. It was found that after immunotherapy, the AR symptom score was reduced, the number of eosinophils in NALF was reduced, and the infiltration of inflammatory cells and tissue damage in the nasal mucosa and lung tissue were alleviated. Immunotherapy can increase the number of CD4+ T cells in the peripheral blood, increase the ratio of CD4+/CD8+ cells, increase the expression of Th1 cytokines such as IL-2 and IFN-γ, reduce the expression of Th2 cytokines such as IL-4 and IL-5. The results showed that repeated intraperitoneal injection of crude extract of HDM for sensitization, followed by nasal drops can effectively construct a mouse model of AR, and subcutaneous injection of immunotherapy in mice can reduce allergic inflammation in model mice and improve the inflammatory infiltration of the nasal cavity in allergic rhinitis. Immunotherapy can reduce the expression of inflammatory factors in AR, improve Th1/Th2 balance, and may play a role in the treatment of AR by improving the function of immune cells.

Loss of SENP3 mediated the formation of nasal polyps in nasal mucosal inflammation by increasing alternative activated macrophage

Small ubiquitin-like modifier (SUMO)-specific protease (SENP)3 is a protease molecule that responds to reactive oxygen species (ROS) with high sensitivity. However, the role of ROS and SENP3 in the formation of nasal polyps (NPs) remains unclear. This study aimed to explore how SENP3 influenced the outcome of chronic rhinosinusitis (CRS) by altering macrophage function, that is, the formation of NPs. The alternative activation of macrophage (M2) was detected with CD68+ CD206+ in humans and CD206+ in mice. The nasal mucosa of patients with CRS was tested using flow cytometry (CD68, CD80, and CD206) and triple-color immunofluorescence staining (CD68, CD206, and SENP3). The bone marrow-derived macrophages from SENP3 knockout and control mice were stimulated with interleukin (IL)-4 and IL-13 to analyze alternative macrophage polarization in vitro. An animal model of allergic rhinitis was constructed using SENP3 knockout mice. CD206 was detected by immunofluorescence staining. The thickening of eosinophil-infiltrated mucosa was detected by Luna staining. The number of CD68+ CD206+ M2 increased in the nasal mucosa of patients with CRS with NP (CRSwNP) compared with patients with CRS without NP (CRSsNP), but with no significant difference between the groups. SENP3 knockout increased the polarization of F4/80+ CD206+ M2. Meanwhile, the number of CD206+ M2 significantly increased in the allergic rhinitis model constructed using SENP3 knockout mice and controls, with a more obvious proliferation of the nasal mucosa. Downregulation of SENP3 promotes the formation of nasal polyps mediated by increasing alternative activated macrophage in nasal mucosal inflammation.

The Effect of Nasal Irrigation with Dewandaru (Eugenia Uniflora L) Leaves Ethanol Extract on Il-4 Levels, Thymic Stromal Lymphopoiethin (TSLP) Expression and Expression of H4 Mucosa Receptors of Wistar Rats with Allergic Rhinitis

Nasal irrigation with Dewandaru leaf extract can reduce inflammatory cell infiltration in the nasal mucosa of rats, and is effective in reducing RA symptoms and has an effect no different from topical corticosteroids. This study aims to prove whether nasal irrigation with ethanolic extract of Dewandaru leaves can reduce the infiltration of allergic inflammatory mediators in the nasal mucosa of male white rats of Wistar strain suffering from RA after ovalbumin nasal spray was induced, by assessing IL-4 levels, TSLP expression and H4 receptor expression. The study was conducted with a randomized post test only control group design, using an animal model of allergic rhinitis, involving 34 male white rats of the Wistar strain, divided into 2, namely: 17 treatment groups and 17 control groups. After 4 weeks of exposure, termination and sampling of rat nasal mucosa was performed. Statistical analysis using the independent sample T test showed that the levels of IL-4 in the nasal mucosa of rats and the expression of H4 receptors on the nasal mucosa of rats were significantly lower than in the control group (p<0.05). Meanwhile, the TSLP expression of the nasal mucosa of rats in the treatment group (2.0154) was not significantly different from the control group (2.1891) with p=0.478, possibly associated with less severe damage to the epithelial barrier cells of the nasal mucosa of TSLP-producing in the group control. The ethanolic extract of Dewandaru leaves has the ability to suppress IL-4 cytokine levels through inhibition of the activity of RH4, so it can be used as a supporting therapy for nasal irrigation that can suppress allergic inflammatory mediators in the nasal mucosa of rats.

Biologic Therapies for Allergic Rhinitis and Nasal Polyposis.

There is an emerging body of research on targeted biologic therapies for the treatment of severe inflammatory nasal disorders, especially chronic rhinosinusitis with nasal polyposis (CRSwNP). This paper will evaluate the efficacy of biologic therapies for severe nasal inflammation by summarizing key preclinical trials of biologics for animal models of allergic rhinitis and the recent phase 2 and 3 clinical trials of biologic therapies for CRSwNP. Biologics that target the IL-4 receptor (dupilumab), IgE (omalizumab), and IL-5 (mepolizumab, reslizumab, and benralizumab) in patients with CRSwNP have shown improvement of various metrics including Sino-Nasal Outcome Test (SNOT-22) scores, Nasal Polyp Scores (NPS), Nasal Congestion Scores (NCS), and Lund-Mackay sinus opacification scores. The efficacy demonstrated through the dupilumab phase 3 trials (LIBERTY NP SINUS-24 and SINUS-52) led to approval of the first biologic for the treatment of CRSwNP. Phase 3 trials for omalizumab (POLYP 1 and 2) and mepolizumab (SYNAPSE study) and post hoc analyses of phase 3 asthma studies for reslizumab and benralizumab have also demonstrated positive results for the use of biologics for patients with CRSwNP. Future efficacy studies and risk/benefit and cost analyses of these biologics and other cytokine targets for allergic rhinitis with and without nasal polyposis need to be performed.

MiR-338–3p inhibits autophagy in a rat model of allergic rhinitis after PM2.5 exposure through AKT/mTOR signaling by targeting UBE2Q1

Exposure to fine particulate matter (PM2.5) increases the incidence of allergic rhinitis (AR). microRNA (miRNA) can regulate cell proliferation, invasion and apoptosis. However, the mechanism of miR-338–3p in mediating PM2.5-induced autophagy in AR animal models remains unknown. To explore the mechanism of miR-338–3p in PM2.5-induced autophagy in AR, the human nasal epithelium cells and AR model exposed to PM2.5 were deployed. The results showed that miR-338–3p was down-regulated in both nasal mucosa of PM2.5-exacerbated AR rat models and PM2.5-treated RPMI-2650 cells. Forced expression of miR-338–3p could inhibit autophagy in vitro. miR-338–3p specifically bound to UBE2Q1 3′-untranslated region (3′ UTR) and negatively regulated its expression. Overexpression of UBE2Q1 attenuated the inhibitory effects of miR-338–3p on PM2.5-induced autophagy of RPMI-2650 cells through AKT/mTOR pathway. Moreover, our in vivo study found that after administration of agomiR-338–3p in AR rats model, the expression of autophagy-related proteins decreased and nasal symptoms alleviated. In conclusion, this study revealed that miR-338–3p acts as an autophagy suppressor in PM2.5-exacerbated AR by directly targeting UBE2Q1 and affecting AKT/mTOR pathway.

Petroleum extract of Farfarae Flos alleviates nasal symptoms by regulating the Th1-Th2 cytokine balance in a mouse model of Allergic Rhinitis.

Farfarae Flos is a traditional Chinese medicine that has long been used to treat allergies. In this study, we aimed to investigate the effect of a petroleum extract of Farfarae Flos (PEFF) in a mouse model of allergic rhinitis (AR) and to explore the underlying molecular mechanisms of action. An animal model of AR was established by sensitization and challenge of BALB/c mice with ovalbumin (OVA). PEFF was administered intranasally and AR nasal symptoms were assessed on a semi-quantitative scale according to the frequencies of nose rubbing and sneezing and the degree of rhinorrhea. The mechanism of action of PEFF was evaluated by histological analysis of nasal mucosa architecture and inflammatory status; ELISA-based quantification of serum OVA-specific IgE, interferon-γ (IFN-γ), and interleukin-4 (IL-4) concentrations; and immunohistochemical and western blot analysis of T-bet and GATA3 protein expression in nasal mucosa and spleen tissues. The results showed intranasal administration of PEFF alleviated AR symptom scores and reduced both the infiltration of inflammatory cells and tissue damage in the nasal mucosa. PEFF significantly decreased serum concentrations of OVA-specific IgE (P<0.01) and IL-4 (P<0.05) and significantly increased IFN-γ (P<0.01). PEFF also upregulated the expression of T-bet protein (P<0.05) but downregulated GATA3 protein (P<0.05) in nasal mucosa and spleen tissues. In conclusion, PEFF effectively reduces AR nasal symptoms and serum IgE levels in a mouse model and may act by correcting the imbalance between Th1 and Th2 responses.

MiR-31 attenuates murine allergic rhinitis by suppressing interleukin-13-induced nasal epithelial inflammatory responses.

The present study aimed to investigate whether microRNA (miR)-31 exerted therapeutic potential in allergic rhinitis (AR) and to explore its underlying mechanism. Firstly, the expression levels of miR-31 were detected by reverse transcription-quantitative PCR in the nasal mucosa of patients and mice. Subsequently, an ovalbumin (OVA)-induced animal model of AR was constructed. Allergic symptom score, histopathological characteristics, OVA-specific immunoglobulin E (IgE) titers, and T-helper (Th)1 and Th2 cell-related cytokine levels were analyzed in OVA-sensitized mice, miR-31-overexpressing mice, miR-negative control mice and control mice. Furthermore, interleukin (IL)-13-stimulated nasal epithelial cells (NECs) were used to assess the effects of miR-31 on the production of IL-13-induced inflammatory cytokines and mucin 5AC by performing western blotting and ELISA. The expression levels of miR-31 were significantly decreased in the nasal mucosa of the AR group compared with those in the control group. Moreover, upregulation of miR-31 markedly attenuated sneezing and nasal rubbing events, reduced nasal eosinophil infiltration and goblet cell hyperplasia, and decreased the levels of OVA-specific IgE and Th2-related cytokines. In addition, subsequent in vitro experiments showed that upregulation of miR-31 inhibited IL-13 receptor α1 chain expression and signal transducer and activator of transcription 6 phosphorylation in NECs. Furthermore, miR-31 suppressed IL-13-induced expression of thymic stromal lymphopoietin, granulocyte-macrophage colony-stimulating factor, eotaxin and mucin 5AC in NECs. In conclusion, these data revealed that miR-31 could ameliorate AR by suppressing IL-13-induced nasal epithelial inflammatory responses, and thus may serve as a novel therapeutic target for AR.

In vitro and in vivo Antiallergic Effects of Taurine on Allergic Rhinitis

Background: The current treatment for allergic rhinitis (AR) is inadequate. Objective: The present study aimed to investigate the therapeutic effect of taurine on AR and to identify the underlying molecular mechanisms. Methods: The serum level of the antioxidant enzyme extracellular superoxide dismutase (SOD3) was determined in AR patients and in healthy controls. The antiallergic inflammatory effects of taurine were evaluated in a dinitrophenyl-human serum albumin (DNP-HSA)-stimulated human mast cell line (HMC-1) and in an ovalbumin (OVA)-induced AR mouse model. Results: Clinically, a reduction in serum level of SOD3 was observed in AR patients. Taurine treatment led to dose-dependent increases in SOD3 at both protein and mRNA levels in HMC-1 cells. SOD3 production was regulated by peroxisome proliferator-activated receptor-γ (PPAR-γ) in response to taurine. SOD3 overexpression inhibited the release of proinflammatory cytokines including tumor necrosis factor-α (, interleukin (IL)-4, and IL-6. Its overexpression also ameliorated the loss of interferon-γ. SOD3 and PPAR-γ influenced inflammatory cytokine production via regulation of the phosphorylation of extracellular signal-regulated kinase 1/2 (ERK1/2). An OVA-induced AR animal model study showed that taurine was efficacious in alleviating allergic inflammatory reactions by relieving behavior symptoms of AR mice and reducing eosinophilic and mast cell infiltration into the nasal cavity. In addition, taurine treatment increased the production of SOD3 and PPAR-γ, which, in turn, suppressed expression of proinflammatory cytokines through phosphorylation of ERK1/2. Conclusion: Taurine could potentially serve as a therapeutic treatment for allergic disorders.

Tripterine: A Potential Anti-Allergic Compound.

Tripterine (TRI), an active monomer in Tripterygium wilfordii, has significant pharmacological activities, such as anti-inflammatory, immunosuppressive and anti-tumor activities. TRI may be used to treat allergic diseases because of its characteristics of immunosuppression. This study aims to explore the anti-allergic effect of TRI. It was tested in vivo and in vitro in this study. The results showed that TRI could significantly inhibit histamine release from rat peritoneal mast cells; the inhibitory effect of TRI on histamine release was stronger than that of other known histamine inhibitors such as disodium cromoglyceride. TRI also significantly inhibited systemic anaphylactic shock induced by compound 48/80 and skin allergy induced by IgE, and inhibited the expression of inflammatory factors secreted by Human Mast Cells (HMC-1) induced by Phorbol 12-Myristate 13- Acetate (PMA) and calcium carrier A23187. In the animal model of allergic rhinitis induced by Ovalbumin (OA), the scores of friction, histamine, IgE, inflammatory factors and inflammatory cells decreased after TRI was administered orally or nasally. TRI, as an active immunoregulatory factor, has great potential in the treatment of mast cell-mediated allergic diseases.

Effect of Biospray Dressings on Eosinophil Infiltration in the Nasal Mucosa and Serum IgE Levels After Nasal Provocation in Experimental Allergic Rhinitis.

PurposeTo investigate the effect of biospray dressing on the extent of eosinophil infiltration in the nasal mucosa and the level of serum IgE in experimental allergic rhinitis with nasal provocation.MethodTwenty-four BALB/c mice were randomly divided into the normal control group, allergic rhinitis (AR) group, dexamethasone (DEX) treatment group, and biospray dressing (BD) group. The mice in the latter 3 groups were prepared for animal models of AR according to standard protocols. Mice in the BD group were administered a nasal spray before the nasal provocation, and those in the DEX group were administered an intraperitoneal injection of DEX. The nasal mucosa and serum were collected from each group. Nasal mucosa eosinophil infiltration was evaluated using hematoxylin and eosin staining, and enzyme-linked immunosorbent assay (ELISA) was performed to analyze the serum IgE expression.ResultsEosinophil infiltration (AR vs BD P = .009) in the nasal mucosa and serum IgE expression (AR vs BD P = .001) were significantly lower in the BD group than in the AR group. There were no significant differences in the extent of eosinophil infiltration in the nasal mucosa or serum IgE expression between the BD and DEX groups.ConclusionBiospray dressings can significantly reduce allergen provocation in the nasal cavity and have a protective effect on the nasal mucosa. They can be used for the prevention and treatment of AR.

Shufengjiedu capsules protect against neuronal loss in olfactory epithelium and lung injury by enhancing autophagy in rats with allergic rhinitis.

Shufengjiedu capsules (SFJDCs), a traditional Chinese medicine, have been widely used as an antiviral, antibacterial, antitumor, and anti-inflammatory drug. However, the roles of SFJDCs in allergic rhinitis remain unclear. The purpose of this study was to investigate the effects of SFJDCs in olfaction and lung injury in rats with allergic rhinitis. An animal model of allergic rhinitis was created by intraperitoneal injection and intranasal administration of ovalbumin to rats. All rats were divided into seven groups: a model group, a low-dose SFJDC group, a medium-dose SFJDC group, a high-dose SFJDC group, a cetirizine group, and a control group. Hematoxylin and eosin (HE) staining was used to observe pathological changes in rat lung and olfactory epithelium (OE) tissue, and peripheral blood was collected and subjected to an enzyme-linked immunosorbent assay (ELISA) to detect IgE, tumor necrosis factor alpha (TNF-α), and IL-1ꞵ levels. Western blotting, immunohistochemistry staining, and immunofluorescence staining were performed to detect inflammatory cytokines and levels of the autophagy biomarker beclin1 and the apoptosis biomarker cleaeved-caspased3 in lung and OE tissue. ELISA indicated that SFJDCs significantly decreased IgE, TNF-α, and IL-1ꞵ levels in peripheral blood, the lungs, and OE tissue. In addition, Western blotting and staining indicated that SFJDCs repair lung injury, protect against neuronal apoptosis in OE, and rescue impaired autophagy in the lungs and OE tissue. In conclusion, results indicated that SFJDCs might protect against neuronal loss in the OE and lung injury by enhancing autophagy and decreasing apoptosis in rats with allergic rhinitis. Therefore, SFJDCs might serve as an alternative treatment for allergic rhinitis.

Distraction of olfactory bulb-medial prefrontal cortex circuit may induce anxiety-like behavior in allergic rhinitis.

Allergic rhinitis is a chronic inflammatory disease of the upper respiratory tract, which is associated with high incidence of anxiety symptom. There is evidence that medial prefrontal cortex modulates anxiety-related behaviors and receives projections from olfactory bulb. Since olfactory dysfunction has been reported in allergic rhinitis, we aimed to evaluate anxiety-like behavior and oscillations of olfactory bulb-medial prefrontal cortex circuit in an animal model of allergic rhinitis. The number of open arm entries in elevated zero maze was significantly reduced in sensitized rats exposed to intranasal ovalbumin compared to the control group, which was indicating the enhancement of anxiety-like behavior in allergic rhinitis animals. Analysis of local field potentials in olfactory bulb and medial prefrontal cortex during immobility and exploration state showed that anxiety-like behavior induced by allergic rhinitis was in association with increased activity of medial prefrontal cortex and enhancement of olfactory bulb-medial prefrontal cortex coupling in delta and theta bands. Moreover, in allergic rhinitis animals, theta strongly coordinates local gamma activity in olfactory bulb and medial prefrontal cortex, which means to have a strong local theta/gamma coupling. We suggested that disruption of olfactory bulb-medial prefrontal cortex circuit due to allergic reactions might have a governing role for inducing anxiety-like behavior in the allergic rhinitis experimental model.

The ameliorative effect of AST2017-01 in an ovalbumin-induced allergic rhinitis animal model.

AST2017-01 is developed to be used for treatment and prevention of allergic diseases and composed of processed-Cordyceps militaris and processed-Rumex crispus. But, effect of AST2017-01 remains unclear in an allergic rhinitis (AR). So, this study aimed to explore the effects of AST2017-01 in ovalbumin (OVA)-induced AR animal model. OVA-induced AR animals were orally administered AST2017-01 and chrysophanol, an active component of AST2017-01 for 10 days. In mice with AR, AST2017-01 and chrysophanol markedly decreased number of rubs, IgE, histamine, thymic stromal lymphopoietin, tumor necrosis factor-α, interleukin (IL)-1β, IL-4, IL-5, and IL-13 in serum or nasal mucosa tissues. Moreover, activities and protein levels of caspase-1 were markedly diminished by oral administration of AST2017-01 and chrysophanol. Declines of macrophage inflammatory protein-2, intercellular adhesion molecules-1, eosinophil, and mast cells were also noted in nasal mucosa tissues of AST2017-01 and chrysophanol groups. Taken together, these findings indicate that AST2017-01 has an anti-allergic effect as a therapeutic agent or functional food for treating and preventing AR.