scholarly journals Apigenin Attenuates Allergic Responses of Ovalbumin-Induced Allergic Rhinitis Through Modulation of Th1/Th2 Responses in Experimental Mice

Dose-Response ◽  
2020 ◽  
Vol 18 (1) ◽  
pp. 155932582090479 ◽  
Author(s):  
Feng Chen ◽  
Dongyun He ◽  
Bailing Yan
Keyword(s):  
Allergic Rhinitis ◽  
Messenger Rna ◽  
Immunoglobulin E ◽  
Elevated Serum ◽  
Lavage Fluid ◽  
Specific Ige ◽  
Cytokine Signaling ◽  
Nuclear Factor ◽  
Th2 Response ◽  
Ifn Γ

Background: Allergic rhinitis (AR) is an immunoglobulin E (IgE)-mediated immune-inflammatory response mainly affecting nasal mucosa. Apigenin, a flavonoid, has been documented to possess promising anti-allergic potential. Aim: To determine the potential mechanism of action of apigenin against ovalbumin (OVA)-induced AR by assessing various behavioral, biochemical, molecular, and ultrastructural modifications. Materials and Methods: Allergic rhinitis was induced in BALB/c mice (18-22 grams) by sensitizing it with OVA (5%, 500 μL, intraperitoneal [IP] on each consecutive day, for 13 days) followed by intranasal challenge with OVA (5%, 5 μL per nostril on day 21). Animals were treated with either vehicle (distilled water, 10 mg/kg, IP) or apigenin (5, 10, and 20 mg/kg, IP). Results: Intranasal challenge of OVA resulted in significant induction ( P < .05) of AR reflected by an increase in nasal symptoms (sneezing, rubbing, and discharge), which were ameliorated significantly ( P < .05) by apigenin (10 and 20 mg/kg) treatment. It also significantly inhibited ( P < .05) OVA-induced elevated serum histamine, OVA-specific IgE, total IgE, and IgG1 and β-hexosaminidase levels. Ovalbumin-induced increased levels of interleukin (IL)-4, IL-5, IL-13, and interferon (IFN)-γ in nasal lavage fluid were significantly decreased ( P < .05) by apigenin. Ovalbumin-induced alterations in splenic GATA binding protein 3 (ie, erythroid transcription factor) (GATA3), T-box protein expressed in T cells (T-bet), signal transducer and activator of transcription-6 (STAT6), suppressor of cytokine signaling 1 (SOCS1), nuclear factor-kappa B (NF-κB), and nuclear factor of kappa light polypeptide gene enhancer in B-cells inhibitor-alpha messenger RNA, as well as protein expressions were significantly inhibited ( P < .05) by apigenin. It also significantly ameliorated ( P < .05) nasal and spleen histopathologic and ultrastructure aberration induced by OVA. Conclusion: Apigenin regulates Th1/Th2 balance via suppression in expressions of Th2 response (IgE, histamine, ILs, GATA3, STAT6, SOCS1, and NF-κB) and activation of Th1 response (IFN-γ and T-bet) to exert its anti-allergic potential in a murine model of OVA-induced AR.

Antidepressant Drug, Desipramine, Alleviates Allergic Rhinitis by Regulating Treg and Th 17 Cells

2013 ◽  
Vol 26 (1) ◽  
pp. 107-115 ◽  
Author(s):  
Y. Zhang ◽  
H. Zhen ◽  
W. Yao ◽  
F. Bian ◽  
X. Mao ◽  
...  
Keyword(s):  
Allergic Rhinitis ◽  
Immunoglobulin E ◽  
Antidepressant Drug ◽  
Flow Cytometric Analysis ◽  
Specific Ige ◽  
Tricyclic Antidepressant ◽  
Interleukin 4 ◽  
Therapeutic Effects ◽  
Nasal Symptoms ◽  
Ifn Γ

Allergic rhinitis (AR) is characterized by IgE-mediated immediate hypersensitivity and usually progresses to chronic nasal inflammation, with depression as one of its comorbidities. The importance of treating the depression in AR patients has been increasingly recognized. Desipramine is a representative of tricyclic-antidepressant agents. In the present study we investigate whether desipramine has therapeutic effects on AR inflammation. BALB/C mice were sensitized by intraperitoneal injection of ovalbumin (OVA), followed by repeated challenge with OVA intranasally. Desipramine was administered orally to treat the mice. The nasal symptoms (sneezing, nasal scratching etc.) of AR were evaluated to determine the severity of AR. Cytokines in the nasal lavage fluid (NALF), including interferon-γ (IFN-γ), interleukin 4 (IL-4) and serum OVA-specific immunoglobulin E (IgE) antibody were measured by ELISA. The regulatory T cells (Treg) and T helper cells 17 (Th17) were quantified by flow cytometric analysis. As a result, the repeated oral administration of desipramine attenuated the nasal symptoms (sneezing and nasal rubbing) in AR mice. Desipramine also suppressed the serum OVA-specific IgE and IL-4 levels, but had no effect on IFN-γ level. Moreover, desipramine treatment up regulated CD4+CD25+Foxp3+Treg cells, which were found down-regulated in established AR mice. Meanwhile, desipramine administration attenuated CD4+IL-17+ Th17 cells, which were significantly increased in AR mice. These results suggest that the antidepressant drug, desipramine, also has anti-allergic action, which was possibly achieved by reducing allergen-specific IgE and Th2 cytokine production and maintaining a balance between Treg and Th17 cells. Thus, this study provide the first evidence that desipramine may be utilized to treat allergic diseases, especially for those allergic patients with depression or depression patients with allergy.

scholarly journals Inhibitory Effects of Urtica thunbergiana Ethanol Extract on Atopic Dermatitis-Induced NC/Nga Mice

Antioxidants ◽  
2020 ◽  
Vol 9 (3) ◽  
pp. 197
Author(s):  
Hien T.T. Ngo ◽  
Minzhe Fang ◽  
Eunson Hwang ◽  
Yoosung Kim ◽  
Bom Park ◽  
...  
Keyword(s):  
Atopic Dermatitis ◽  
Immunoglobulin E ◽  
Elevated Serum ◽  
Nuclear Factor ◽  
Hacat Cells ◽  
Tnf Α ◽  
Ifn Γ ◽  
Urtica Thunbergiana

Atopic dermatitis (AD) is a chronic, inflammatory skin disease that persists or repeatedly recurs in both childhood and adulthood. Urtica thunbergiana (UT) is an aroma herb with little-known pharmacological effects and anti-inflammatory activities against AD. This study investigated the immunomodulatory efficacy of 50% ethanol-extracted UT in necrosis factor-alpha/interferon-gamma (TNF-α/IFN-γ)-stimulated HaCaT cells in vitro and AD-Biostir-induced NC/Nga mice in vivo. The results showed that UT exhibits a dose-dependent increase in scavenged free radicals, reaching 76.0% ± 1.4% of scavenged 1,1-diphenyl-2-picrylhydrazyl at a concentration of 250 µg/mL. In addition, UT significantly downregulated the mRNA expression of the following pro-inflammatory cytokines and chemokines in TNF-α/IFN-γ-stimulated HaCaT cells: interleukin (IL)-6, IL-8, thymus- and activation-regulated chemokine, macrophage-derived chemokine, and regulated on activation normal T expressed and secreted. UT-treated HaCaT cells showed inhibition of the overexpression of chemokine-regulated signaling molecules, such as nuclear factor-kappa B, inhibitor of kappa B (IκBα), signal transducer and activator of transcription 1, and mitogen-activated protein kinases (MAPKs). UT dietary administration in AD-Biostir-induced NC/Nga mice treated and improved AD-like symptoms, such as scales, epidermal thickening, the dermatitis severity score, high trans-epidermal water loss, reduced skin hydration, increased mast cells, elevated serum immunoglobulin E levels, and an enlarged spleen. UT treatment inhibited the expression of phosphorylated forms of MAPKs, nuclear factor of activated T-cells 1, and regulator IκBα. It also upregulated filaggrin (FLG) production. Therefore, UT shows high anti-AD activity both in vitro and in vivo, and can be a useful anti-AD agent.

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.

scholarly journals Anti-inflammatory effect of wogonin on allergic responses in ovalbumin-induced allergic rhinitis in the mouse

2018 ◽  
Vol 9 ◽  
pp. 215265671876414 ◽  
Author(s):  
Kyeong Ah Kim ◽  
Joo Hyun Jung ◽  
Yun Sook Choi ◽  
Gyu Kang ◽  
Seon Tae Kim
Keyword(s):  
Allergic Rhinitis ◽  
Immunoglobulin E ◽  
Allergic Diseases ◽  
Serum Levels ◽  
Lavage Fluid ◽  
Specific Ige ◽  
Eosinophil Infiltration ◽  
Treatment Groups ◽  
Specific Immunoglobulin E ◽  
Group A

Background Wogonin is commonly used for the treatment of allergic diseases. However, neither its precise effect in preventing allergic rhinitis (AR) nor its mechanism of action are known. Objectives In this study, the effect of wogonin on allergic responses in ovalbumin (OVA) induced AR was investigated in mice. Methods BALB/c mice were sensitized with intraperitoneal (i.p.) OVA and then challenged intranasally with OVA. Wogonin (10 and 30 mg/kg) was given to the treatment groups, and the effect of wogonin on the release of allergic inflammatory mediators, specifically OVA-specific immunoglobulin E (IgE) and inflammatory cytokines, was explored. Eosinophil infiltration and the levels of interleukin (IL) 5 and IL-13 were measured by immunohistochemistry. Results In mice with AR, wogonin decreased OVA-specific IgE levels in serum, and the levels of the cytokines IL-4, IL-5, IL-13, eotaxin, and RANTES in nasal lavage fluid. Serum levels of IL-4, IL-5, and IL-13 were lower in both groups of wogonin-pretreated mice than in the OVA group. A reduction in eosinophil infiltration of the nasal mucosa and inhibition of the expression of IL-5 and IL-13 were also noted in the treated groups. Conclusion Wogonin induced antiallergic effects in a murine model of AR by decreasing the infiltration of eosinophils and levels of T-helper type 2 cytokines. Thus, wogonin merits consideration as a therapeutic agent for treating AR.

Mechanism of miR-181a-5p in Regulatory T/T-Helper 17 Immune Imbalance and Asthma Development in Mice with Allergic Rhinitis

2021 ◽  
pp. 1-14
Author(s):  
Ruoyun He ◽  
Yujuan Chen ◽  
Xiaoer Chen ◽  
Binfan Yuan
Keyword(s):  
Allergic Rhinitis ◽  
Immunoglobulin E ◽  
High Mobility ◽  
Lavage Fluid ◽  
Chromosomal Protein ◽  
T Helper ◽  
T Helper 17 ◽  
Immune Disorder ◽  
Ifn Γ ◽  
Immune Imbalance

<b><i>Introduction:</i></b> Allergic rhinitis (AR) is an immune disorder and also a risk factor of asthma. microRNAs (miRNAs) are implicated in autoimmune diseases, including RA. This study investigated effect of miR-181a-5p on regulatory T (Treg)/ T-helper (Th) 17 immune imbalance in AR. <b><i>Methods:</i></b> A murine model of AR was established and treated with lentivirus modified miR-181a-5p. The allergic symptoms of mice were examined. The contents of Th17-related cytokines (interferon [IFN]-γ and interleukin [IL]-6), Treg-related cytokine (IL-10), and Treg-specific nuclear transcription factor (Foxp3) in nasal mucosa and lung tissues were determined. The proportion of Treg and Th17 cells was analyzed by flow cytometry. The level of ovalbumin-specific immunoglobulin E in the serum, and the contents of IL-4, IL-5, and IL-13 in bronchoalveolar lavage fluid and IFN-γ, IL-6, and IL-10 in nasal lavage fluid were measured. The targeting relationship between miR-181a-5p and high mobility group box chromosomal protein 1 (HMGB1) was verified. HMGB1 and receptor for advanced glycation end products (RAGE) expression in RA were determined, and the interaction between HMGB1 and RAGE was detected. <b><i>Results:</i></b> miR-181a-5p expression was reduced in AR mice. miR-181a-5p overexpression attenuated allergic behaviors, alleviated Treg/Th17 imbalance, and delayed asthma development. HMGB1 and RAGE were elevated in AR mice. miR-181a-5p targeted HMGB1, and HMGB1 bound to RAGE, while miR-181a-5p overexpression reduced the binding between them. Activating HMGB1/RAGE reversed the protective effect of miR-181a-5p overexpression on AR and induced the development of asthma. <b><i>Conclusion:</i></b> miR-181a-5p overexpression reduced the binding of HMGB1 and RAGE by inhibiting HMGB1, thus alleviating Treg/Th17 immune imbalance and blocking AR from developing into asthma.

scholarly journals MicroRNA-182-5p relieves murine allergic rhinitis via TLR4/NF-κB pathway

Open Medicine ◽  
2020 ◽  
Vol 15 (1) ◽  
pp. 1202-1212
Author(s):  
Aichun Zhang ◽  
Yangzi Jin
Keyword(s):  
Allergic Rhinitis ◽  
Inflammatory Cells ◽  
Lavage Fluid ◽  
Specific Ige ◽  
Inflammatory Factors ◽  
Pcr Analysis ◽  
Reverse Transcription Pcr ◽  
Pathway Activation ◽  
Nasal Lavage Fluid

AbstractAllergic rhinitis (AR) is one of the most common chronic diseases. This study examined whether microRNA (miR)-182-5p plays a role in AR by regulating toll-like receptor 4 (TLR4). First, data demonstrated that TLR4 was a target of miR-182-5p. Subsequently, AR mouse model was established to explore the role of miR-182-5p and TLR4 in AR in vivo. Initially, quantitative reverse transcription-PCR (qRT-PCR) analysis indicated that miR-182-5p was downregulated, while TLR4 expression was upregulated in AR mice. Then we found that miR-182-5p mimic reduced the frequency of sneezing and nose rubbing of the AR mice. In addition, miR-182-5p mimic significantly increased ovalbumin (OVA)-specific IgE and leukotriene C4 expression levels in nasal lavage fluid (NLF) and serum of AR mice. miR-182-5p mimic decreased the number of inflammatory cells in NLF of AR mice. It also reduced the levels of inflammatory factors in the serum of AR mice, such as interleukin (IL)-4, IL-5, IL-13, IL-17 and tumor necrosis factor (TNF)-α, while increasing the release of IFN-γ and IL-2. Finally, miR-182-5p mimic inhibited NF-κB signaling pathway activation in AR mice. However, all effects of miR-182-5p mimic on AR mice were reversed by TLR4-plasmid. In conclusion, miR-182-5p/TLR4 axis may represent a novel therapeutic target for AR.

scholarly journals Co-exposure to lipopolysaccharide and desert dust causes exacerbation of ovalbumin-induced allergic lung inflammation in mice via TLR4/MyD88-dependent and -independent pathways

2019 ◽  
Vol 15 (1) ◽  
Author(s):  
Yahao Ren ◽  
Takamichi Ichinose ◽  
Miao He ◽  
Seiichi Youshida ◽  
Masataka Nishikawa ◽  
...  
Keyword(s):  
Airway Inflammation ◽  
Immune Cell ◽  
Adaptor Protein ◽  
Lavage Fluid ◽  
Specific Ige ◽  
Pathological Changes ◽  
Th2 Response ◽  
Lung Eosinophilia ◽  
High Concentrations

Abstract Background Lipopolysaccharide (LPS) often presents in high concentrations in particulate matter (PM), few studies have reported the enhancing effects of both LPS and PM on airway inflammation in mice and the role of toll-like receptors (TLRs) in this process. Asian sand dust (ASD) is observed most frequently during the spring. This study aimed to clarify the role of TLRs in murine lung eosinophilia exacerbated by ASD and LPS. Methods The effects of LPS and ASD co-treatment on ovalbumin (OVA)-induced lung eosinophilia were investigated using wild-type (WT), TLR2−/−, TLR4−/−, and adaptor protein myeloid differentiation factor 88 (MyD88)−/− BALB/c mice. ASD was heated (H-ASD) to remove the toxic organic substances. WT, TLR2−/−, TLR4−/− and MyD88−/− BALB/c mice were intratracheally instilled with four different combinations of LPS, H-ASD and OVA treatment. Subsequently, the pathological changes in lungs, immune cell profiles in bronchoalveolar lavage fluid (BALF), inflammatory cytokines/chemokines levels in BALF and OVA-specific immunoglobulin (Ig) in serum were analyzed. Results In WT mice, H-ASD + LPS exacerbated OVA-induced lung eosinophilia. This combination of treatments increased the proportion of eosinophils and the levels of IL-5, IL-13, eotaxin in BALF, as well as the production of OVA-specific IgE and IgG1 in serum compared to OVA treatment alone. Although these effects were stronger in TLR2−/− mice than in TLR4−/− mice, the expression levels of IL-5, IL-13, eotaxin were somewhat increased in TLR4−/− mice treated with OVA + H-ASD + LPS. In MyD88−/− mice, this pro-inflammatory mediator-induced airway inflammation was considerably weak and the pathological changes in lungs were negligible. Conclusions These results suggest that LPS and H-ASD activate OVA-induced Th2 response in mice, and exacerbate lung eosinophilia via TLR4/MyD88, TLR4/TRIF and other TLR4-independent pathways.

Bifidobacterium longum IM55 and Lactobacillus plantarum IM76 alleviate allergic rhinitis in mice by restoring Th2/Treg imbalance and gut microbiota disturbance

2019 ◽  
Vol 10 (1) ◽  
pp. 55-67 ◽  
Author(s):  
W.-G. Kim ◽  
G.-D. Kang ◽  
H.I. Kim ◽  
M.J. Han ◽  
D.-H. Kim
Keyword(s):  
T Cells ◽  
Allergic Rhinitis ◽  
Regulatory T Cells ◽  
Gut Microbiota ◽  
Lactobacillus Plantarum ◽  
Immunoglobulin E ◽  
Bifidobacterium Longum ◽  
Lavage Fluid ◽  
Th2 Cells

This study aimed to examine whether probiotics, which suppressed the differentiation of splenic T cells into type 2 helper T (Th2) cells and induced into regulatory T cells in vitro, alleviate allergic rhinitis (AR) and gut microbiota disturbance. We isolated Bifidobacterium longum IM55 and Lactobacillus plantarum IM76 from human faecal microbiota and kimchi, respectively, and examined their effects on ovalbumin (OVA)-induced AR and gut microbiota disturbance in mice. Treatment with IM55, IM76, or their probiotic mixture (PM) significantly reduced OVA-induced allergic nasal symptoms and blood immunoglobulin E (IgE) levels in mice. These also reduced OVA-induced interleukin (IL)-4 and IL-5 levels in nasal tissues and bronchoalveolar lavage fluid (BALF) but increased OVA-suppressed IL-10 levels. Treatment with IM55, IM76, or PM reduced OVA-induced increase in the populations of mast cells, eosinophils, and Th2 cells and increased OVA-suppressed population of regulatory T cells in the BALF. Treatment with IM55, IM76, or PM also inhibited OVA-induced expression of IL-5 in lung and colon tissues and restored OVA-disturbed composition of gut microbiota Proteobacteria, Bacteroidetes, and Actinobacteria. These results suggest that IM55 and IM67 can alleviate AR by restoring Th2/Treg imbalance and gut microbiota disturbance.

scholarly journals Honeysuckle extract relieves ovalbumin-induced allergic rhinitis by inhibiting AR-induced inflammation and autoimmunity

2019 ◽  
Vol 39 (7) ◽  
Author(s):  
Bin Lin ◽  
Bijuan Cai ◽  
Huige Wang
Keyword(s):  
Allergic Rhinitis ◽  
Nasal Mucosa ◽  
Inflammatory Reaction ◽  
Lavage Fluid ◽  
Nasal Lavage ◽  
Autoimmune Response ◽  
Enzyme Linked Immunosorbent Assay ◽  
Protein Levels ◽  
Nasal Lavage Fluid ◽  
Ifn Γ

Abstract Honeysuckle has antiviral, antioxidative and anti-inflammatory properties. Allergic rhinitis (AR) is induced by immunoglobulin E (IgE)-mediated inflammatory reaction. Our study investigates whether honeysuckle extract (HE) has therapeutic effect on AR. An AR model of mice was established by ovalbumin (OVA). Hematoxylin–Eosin staining was used to assess nasal mucosa damage. Enzyme-linked immunosorbent assay (ELISA) was performed to determine serum histamine, IgE and interleukin (IL)-2, IL-4, IL-17 and interferon-γ (IFN-γ) from nasal lavage fluid. Western blot was carried out to analyze the protein level from nasal mucosa tissue. We found that HE not only decreased nasal rubbing and sneezing in AR mice, but also reduced AR-induced damage to nasal mucosa. Moreover, HE lowered the levels of serum IgE and histamine and inhibited IL-4 and IL-17 levels from AR mice but raised IL-2 and IFN-γ levels in AR-induced nasal lavage fluid. Our results also showed that HE elevated the protein levels of forkhead box P3 (Foxp3) and T-box transcription factor (T-bet) in AR-induced nasal mucosa tissue, whereas it inhibited signal transducer and activator of transcription (STAT) 3 and GATA binding protein 3 (GATA-3) protein levels. By regulating AR-induced inflammatory reaction and autoimmune response, HE also relieved OVA-induced AR. Thus, HE could be used as a potential drug to treat AR.

Paeonol attenuates airway inflammation and hyperresponsiveness in a murine model of ovalbumin-induced asthma

2010 ◽  
Vol 88 (10) ◽  
pp. 1010-1016 ◽  
Author(s):  
Qiang Du ◽  
Gan-Zhu Feng ◽  
Li Shen ◽  
Jin Cui ◽  
Jian-Kang Cai
Keyword(s):  
Bronchoalveolar Lavage ◽  
Airway Inflammation ◽  
Bronchoalveolar Lavage Fluid ◽  
Immunoglobulin E ◽  
Therapeutic Potential ◽  
Lavage Fluid ◽  
Interleukin 4 ◽  
Moutan Cortex ◽  
Ifn Γ ◽  
Anti Inflammatory

Paeonol, the main active component isolated from Moutan Cortex, possesses extensive pharmacological activities such as anti-inflammatory, anti-allergic, and immunoregulatory effects. In the present study, we examined the effects of paeonol on airway inflammation and hyperresponsiveness in a mouse model of allergic asthma. BALB/c mice sensitized and challenged with ovalbumin were administered paeonol intragastrically at a dose of 100 mg/kg daily. Paeonol significantly suppressed ovalbumin-induced airway hyperresponsiveness to acetylcholine chloride. Paeonol administration significantly inhibited the total inflammatory cell and eosinophil count in bronchoalveolar lavage fluid. Treatment with paeonol significantly enhanced IFN-γ levels and decreased interleukin-4 and interleukin-13 levels in bronchoalveolar lavage fluid and total immunoglobulin E levels in serum. Histological examination of lung tissue demonstrated that paeonol significantly attenuated allergen-induced lung eosinophilic inflammation and mucus-producing goblet cells in the airway. These data suggest that paeonol exhibits anti-inflammatory activity in allergic mice and may possess new therapeutic potential for the treatment of allergic bronchial asthma.

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