scholarly journals Effects of Laminaria japonica polysaccharides on airway inflammation of lungs in an asthma mouse model

2015 ◽  
Vol 10 ◽  
Author(s):  
Rongjun Lin ◽  
Xiaomei Liu ◽  
Yan Meng ◽  
Mei Xu ◽  
Jianping Guo
Keyword(s):  
Airway Inflammation ◽  
Laminaria Japonica ◽  
Inflammatory Cells ◽  
Serum Levels ◽  
Lavage Fluid ◽  
Chronic Inflammatory Disease ◽  
Serum Ige ◽  
Asthma Model ◽  
Group A ◽  
Tgf Β1

Background: Asthma is a serious chronic inflammatory disease affecting 300 million people worldwide. This aim of this study to investigate the anti-inflammatory and anti-asthmatic effects of Laminaria japonica extract in the ovalbumin (OVA)-induced mouse asthma model. Methods: A mouse asthma model was established in SPF Kunming mice by OVA-sensitization followed by inhalation of aerosol allergen for two weeks. Laminaria japonica polysaccharides (LJPS) were given by gavage feeding at 50 mg/kg/day during OVA inhalation challenge period, and their effect on asthma was compared with the standard treatment of Budesonide inhalation. The total inflammatory cells and eosinophils in bronchoalveolar lavage fluid (BALF) were determined. Histopathological changes in lung tissue were studied and scored to determine the degree of inflammation. Levels of IL-12, IL-13, and TGF-β1 in BALF as well as serum levels of IgE were measured. Expressions of IL-12, IL-13, and TGF-β1 in lung tissues were assessed. Results: Highly inflammatory lungs infiltrated with significant increased eosinophils were observed in OVAinduced asthmatic mice. The OVA treated mice presented with a lower level of IL-12 and higher levels of IL-13 and TGF-β1 in BALF and lung tissues, as well as an increased level of the serum IgE. Treatment with LJPS (Group B) significantly decreased the numbers of eosinophils in the BALF (P<0.05) and alleviated lung inflammation compared to the untreated asthma mice (Group A). It also reduced the serum IgE levels, increased expression of IL-12, and decreased the expression of IL-13 and TGF-β1 in BALF and lung (Both P < 0.05) compared with the group A. Conclusions: LJPS can significantly inhibit airway inflammation of asthmatic mice, adjust the balance of cytokines, and improve the pulmonary histopathological condition. Our data suggested that LJPS might be a potential therapeutic reagent for allergic asthma.

scholarly journals Paeonol Ameliorates Ovalbumin-Induced Asthma through the Inhibition of TLR4/NF-κB and MAPK Signaling

2018 ◽  
Vol 2018 ◽  
pp. 1-8 ◽  
Author(s):  
Yongjun Tang ◽  
Weihua Huang ◽  
Qianqian Song ◽  
Xiangrong Zheng ◽  
Ruohui He ◽  
...  
Keyword(s):  
Nuclear Translocation ◽  
Inflammatory Cells ◽  
Underlying Mechanism ◽  
Lavage Fluid ◽  
Mapk Signaling ◽  
Chronic Inflammatory Disease ◽  
Mitogen Activated Protein Kinase ◽  
Asthma Model ◽  
Mitogen Activated Protein ◽  
Complex Signaling

Asthma is a chronic inflammatory disease of the airways, with complex signaling pathways involved in its pathogenesis. It was reported that paeonol attenuated airway inflammation of ovalbumin (OVA)-induced mice. Therefore, it is of importance to further investigate the underlying mechanism. BALB/c mice were challenged with OVA for the asthma model, which was validated by the changed levels of IL-4, IFN-γ, and IgE. The elevation of IL-4 and the decreasing of IFN-γ were significantly in middle (p<0.05) or high (p<0.01) paeonol dose groups compared with OVA group. MIP-1β in bronchoalveolar lavage fluid (BALF) also decreased significantly in middle and high paeonol group compared with OVA group (p<0.01), which is similar to the change of its mRNA in lung tissues. Moreover, the inflammatory cells infiltration and collagen deposition were attenuated by paeonol and montelukast sodium via histology examination. At last the immune blot of the protein extracted from lung tissues demonstrated that paeonol decreased the expression of TLR4 and the nuclear translocation of NF-κB, as well as the phosphorylation levels of P38 and ERK in asthma model. In conclusion, paeonol ameliorated OVA-induced asthma through the TLR4/NF-κB and mitogen-activated protein kinase (MAPK) signaling.

scholarly journals Effects of caffeoylxanthiazonoside on airway inflammation in an allergic asthma mice model

2021 ◽  
Vol 18 (4) ◽  
pp. 761-766
Author(s):  
Qian Wu ◽  
Hui Wang ◽  
Xiaowen Che ◽  
Wei Wang
Keyword(s):  
Protein Expression ◽  
Western Blot ◽  
Airway Inflammation ◽  
Allergic Asthma ◽  
Inflammatory Cells ◽  
Lavage Fluid ◽  
The Body ◽  
Enzyme Linked Immunosorbent Assay ◽  
Mice Model ◽  
Ifn Γ

Purpose: To investigate the inhibitory effects of caffeoylxanthiazonoside (CYT) on airway inflammation in mice and its mechanism of action. Methods: An allergic asthma mice model was established by intraperitoneal injection and aerosol nebulization with ovalbumin (OVA). After treatment with CYT, the blood and bronchoalveolar lavage fluid (BALF) were collected from the mice. The leukocytes were classified and counted with Giemsa solution. Enzyme-linked immunosorbent assay (ELISA) was used to determine the serum levels of IgE, and IL-4, IL-5, IL-13 and IFN-γ in the BALF of mice. Lung tissues were obtained from the mice and MUC5AC protein expression was measured by western blot. Results: CYT significantly decreased the serum level of IgE in asthmatic mice. Inflammatory cells in BALF of mice were markedly reduced (p < 0.05) by CYT treatment at varying doses (10, 20, and 40 mg/kg). Treatment with CYT also significantly suppressed the cytokines of IL-4, IL-5 and IL-13 and increased the IFN-γ in the BLAF of OVA-induced allergic asthma mice (p < 0.05). Western blot results indicate that CYT treatment significantly decreased the expression of MUC5AC protein in the lung tissues of asthmatic mice. In addition, no significant effects on the body weight of the mice were found after CYT treatment. Conclusion: Caffeoylxanthiazonoside inhibits airway inflammation in allergic asthma mice by altering Th1/Th2 via re-balancing of related cytokines and downregulation of lung MUC5AC protein expression. Therefore, this compound can potentially be developed for the therapeutic management of inflammation in allergic asthma.

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 Neonatal Streptococcus pneumoniae Pneumonia Induces an Aberrant Airway Smooth Muscle Phenotype and AHR in Mice Model

2019 ◽  
Vol 2019 ◽  
pp. 1-8 ◽  
Author(s):  
Xin Peng ◽  
Yi Wu ◽  
Xiao Kong ◽  
Yunxiu Chen ◽  
Yonglu Tian ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Streptococcus Pneumoniae ◽  
Airway Inflammation ◽  
Allergic Asthma ◽  
Airway Smooth Muscle ◽  
Airway Hyperresponsiveness ◽  
Inflammatory Cells ◽  
Pivotal Role ◽  
Mice Model ◽  
Asthma Model

Our previous study showed that neonatal S. pneumoniae infection aggravated airway inflammation and airway hyperresponsiveness (AHR) in an OVA-induced allergic asthma model. As airway smooth muscle (ASM) plays a pivotal role in AHR development, we aim to investigate the effects of neonatal S. pneumoniae pneumonia on ASM structure and AHR development. Non-lethal neonatal pneumonia was established by intranasally infecting 1-week-old BALB/C mice with the S. pneumoniae strain D39. Five weeks after infection, the lungs were collected to assess the levels of α-SMA and the contractile proteins of ASM. Our results indicate that neonatal S. pneumoniae pneumonia significantly increased adulthood lung α-SMA and SMMHC proteins production and aggravated airway inflammatory cells infiltration and cytokines release. In addition, the neonatal S. pneumoniae pneumonia group had significantly higher Penh values compared to the uninfected controls. These data suggest that neonatal S. pneumoniae pneumonia promoted an aberrant ASM phenotype and AHR development in mice model.

Montelukast prevents the decrease of interleukin-10 and inhibits NF-κB activation in inflammatory airway of asthmatic guinea pigs

2006 ◽  
Vol 84 (5) ◽  
pp. 531-537 ◽  
Author(s):  
Yuqing Wu ◽  
Chenghua Zhou ◽  
Jin Tao ◽  
Shengnan Li
Keyword(s):  
Airway Inflammation ◽  
Guinea Pigs ◽  
Gradient Centrifugation ◽  
Pulmonary Inflammation ◽  
Lavage Fluid ◽  
Nuclear Factor Κb ◽  
Interleukin 10 ◽  
High Dose ◽  
Model Group ◽  
Asthma Model

Interleukin (IL)-10 is an important immunoregulatory and anti-inflammatory cytokine, whereas nuclear factor-κB (NF-κB) plays an important role in the pathogenesis of asthma. In the present study, the effects of montelukast on the level of IL-10 and on the activation of NF-κB in the inflammatory airway of asthmatic guinea pigs were investigated. Guinea pigs were sensitized by ovalbumin. Pulmonary inflammation was observed by hematoxylin and eosin staining. The eosinophils in broncho-alveolar lavage fluid and blood were separated by density gradient centrifugation and counted under microscope. The level of IL-10 in broncho-alveolar lavage fluid was measured by enzyme-linked immunoadsorbent assay. Activation of NF-κB in lung tissues was inspected by immunohistochemistry. Montelukast at medium and high doses prevented the decrease of IL-10 in broncho-alveolar lavage fluid (n = 8, p < 0.01 vs. asthma model group), inhibited the activation of NF-κB in lung tissues (n = 8; medium dose, p < 0.05; high dose, p < 0.01; vs. asthma model group). There was a significantly negative correlation between the level of IL-10 and the activation of NF-κB in lung tissues (r = –0.488, p < 0.01). Montelukast reduced the severity of airway inflammation and the number of eosinophils in asthmatic guinea pigs. From all these findings we conclude that montelukast can prevent the decrease of IL-10 and inhibit the activation of NF-κB in inflammatory airway of asthmatic guinea pigs, which may be the new important mechanisms of montelukast’s anti-airway-inflammation effects in asthmatic guinea pigs.

scholarly journals Alnus hirsuta (Spach) Rupr. Attenuates Airway Inflammation and Mucus Overproduction in a Murine Model of Ovalbumin-Challenged Asthma

2021 ◽  
Vol 12 ◽  
Author(s):  
Ba-Wool Lee ◽  
Ji-Hye Ha ◽  
Yeongseon Ji ◽  
Seong-Hun Jeong ◽  
Ju-Hong Kim ◽  
...  
Keyword(s):  
Airway Inflammation ◽  
Allergic Asthma ◽  
Immunoglobulin E ◽  
Inflammatory Cells ◽  
Lavage Fluid ◽  
Th2 Cytokines ◽  
Protective Effects ◽  
Mucus Production ◽  
Tnf Α ◽  
Alnus Hirsuta

Alnus hirsuta (Spach) Rupr. (AH), a member of the Betulaceae family, is widely used in Eastern Asia of as a source of medicinal compounds for the treatment of hemorrhage, diarrhea, and alcoholism. In this study, we investigated the protective effects of a methanolic extract of AH branches against airway inflammation and mucus production in tumor necrosis factor (TNF)-α-stimulated NCI-H292 cells and in an ovalbumin (OVA)-challenged allergic asthma mouse model. Female BALB/c mice were injected with OVA (40 μg) and aluminum hydroxide (2 mg) on days 0 and 14 to induce allergic airway inflammation. The mice were then challenged with 1% OVA from days 21–23. Mice were treated with AH (50 and 100 mg/kg/day; 2% DMSO) or dexamethasone (positive control; 3 mg/kg/day) from days 18–23. AH treatment effectively attenuated airway resistance/hyperresponsiveness and reduced levels of T helper type 2 (Th2) cytokines, eotaxins, and number of inflammatory cells in bronchoalveolar lavage fluid, and immunoglobulin E in serums of OVA-challenged mice. In histological analysis, AH treatment significantly inhibited airway inflammation and mucus production in OVA-challenged mice. AH treatment downregulated the phosphorylation of I kappa B-alpha, p65 nuclear factor-kappa B (p65NF-κB), and mitogen-activated protein kinases with suppression of mucin 5AC (MUC5AC) in lung tissue. Moreover, AH treatment decreased the levels of pro-inflammatory cytokines and Th2 cytokines, as well as MUC5AC expression, and inhibited the phosphorylation of p65NF-κB in TNF-α-stimulated NCI-H292 cells. These results indicate that AH might represent a useful therapeutic agent for the treatment of allergic asthma.

Effect of the Fungal Immunomodulatory Protein FIP-fve in the Neutrophilic Asthma Animal Model

2021 ◽  
pp. 1-12
Author(s):  
Hui-Hsien Pan ◽  
Jiunn-Liang Ko ◽  
Chia-Ta Wu ◽  
Hai-Lun Sun ◽  
Yeak-Wun Quek ◽  
...  
Keyword(s):  
Airway Inflammation ◽  
Transforming Growth Factor ◽  
Inflammatory Cells ◽  
Neutrophil Infiltration ◽  
Transforming Growth Factor Β ◽  
Lavage Fluid ◽  
Fungal Immunomodulatory Protein ◽  
Hematoxylin And Eosin ◽  
Ifn Γ ◽  
Hematoxylin And Eosin Stain

<b><i>Background:</i></b> Asthma animal models provide valuable information about the pathogenesis and the treatment of asthma. An ovalbumin (OVA)/complete Freund’s adjuvant (CFA)-sensitized model was developed to induce neutrophil-dominant asthma and to investigate whether fungal immunomodulatory peptide-<i>fve</i> (FIP-<i>fve</i>) could improve asthma features in the OVA/CFA-sensitized model. <b><i>Methods:</i></b> We used female BALB/c mice and sensitized them intraperitoneally with OVA/CFA on days 1, 2, and 3. On days 14, 17, 21, 24, and 27, they were challenged with intranasal OVA. The airway hyper-responsiveness (AHR) was detected by BUXCO, inflammatory cells were stained with Liu’s stain, the cytokines were detected using ELISA, and the airway inflammation was analyzed with hematoxylin and eosin stain. <b><i>Results:</i></b> According to the results, OVA/CFA sensitization could induce AHR, high levels of IgE, and inflammatory cells especially neutrophils infiltration in the lung and airway inflammation. IL-4, IL-5, IL-6, IL-8, IL-10, IL-13, IL-17, IL-25, IL-33, and transforming growth factor-β (TGF-β) increased in the OVA/CFA-sensitized mice. OVA/CFA-sensitized mice treated with FIP-<i>fve</i> not only increased IL-12 and IFN-γ but also decreased IL-4, IL-5, IL-6, IL-8, IL-13, IL-17, IL-25, IL-33, and TGF-β in the bronchoalveolar lavage fluid. Moreover, FIP-<i>fve</i> significantly decreased neutrophil infiltration in the lung. <b><i>Conclusion:</i></b> The OVA/CFA model induced neutrophilic asthma successfully, and FIP-<i>fve</i> improved neutrophil-dominant asthma.

scholarly journals Sequential expression of IGF-IB followed by active TGF-β1 induces synergistic pulmonary fibroproliferation in vivo

2012 ◽  
Vol 303 (9) ◽  
pp. L788-L798 ◽  
Author(s):  
Graciela Andonegui ◽  
Ai Ni ◽  
Caroline Léger ◽  
Margaret M. Kelly ◽  
Josée F. Wong ◽  
...  
Keyword(s):  
Pulmonary Fibrosis ◽  
Ex Vivo ◽  
Smooth Muscle Actin ◽  
Wild Type Mouse ◽  
Inflammatory Cells ◽  
Lung Parenchyma ◽  
Lavage Fluid ◽  
Igf I ◽  
Tgf Β1

Pulmonary fibrosis, the end stage of a variety of fibroproliferative lung diseases, is usually induced after repetitive or chronic lung injury or inflammation. The mechanisms of fibroproliferation are poorly understood. Insulin-like growth factor-I (IGF-I) is significantly elevated in patients with pulmonary fibrosis and fibroproliferative acute respiratory distress syndrome. However, we showed that IGF-I overexpression alone in wild-type mouse lungs does not cause fibroproliferation. We therefore questioned whether IGF-I, acting together with active TGF-β1, a known profibrotic cytokine, enhances pulmonary fibroproliferation caused by active TGF-β1. A unique sequential adenoviral transgene mouse model was used expressing AdEmpty/AdTGF-β1 or AdhIGF-IB/AdTGF-β1 transgenes. IGF-IB plus active TGF-β1 transgene expression synergistically increased collagen deposition in the lung parenchyma compared with active TGF-β1 expression alone. The enhanced fibrosis was accompanied by an increased recruitment of macrophages and lymphocytes into the bronchoalveolar lavage fluid (BALF) and inflammatory cells in the lungs. α-Smooth muscle actin expression, a marker of myofibroblast proliferation and differentiation, was also increased. Finally, fibroblasts exposed ex vivo to BALF isolated from AdhIGF-IB/AdTGF-β1-transduced mice showed synergistic collagen induction compared with BALF from AdEmpty/AdTGF-β1-transduced mice. This study provides the first direct evidence that IGF-I is able to synergistically enhance pulmonary fibroproliferation in cooperation with TGF-β1.

scholarly journals The non-antibiotic macrolide EM900 attenuates HDM and poly(I:C)-induced airway inflammation with inhibition of macrophages in a mouse model

2019 ◽  
Vol 69 (1) ◽  
pp. 139-151 ◽  
Author(s):  
Hironori Sadamatsu ◽  
Koichiro Takahashi ◽  
Hiroki Tashiro ◽  
Go Kato ◽  
Yoshihiko Noguchi ◽  
...  
Keyword(s):  
Airway Inflammation ◽  
Bronchoalveolar Lavage Fluid ◽  
Allergic Airway Inflammation ◽  
Inflammatory Cells ◽  
Lavage Fluid ◽  
Poly I:C ◽  
Inhibitory Effects ◽  
Polycytidylic Acid ◽  
Bacterial Drug Resistance ◽  
Dust Mite

Abstract Objective Macrolides have been reported to reduce the exacerbation of severe asthma. The aim of this study was to clarify the effects and mechanisms of EM900, a non-antibiotic macrolide, on allergic airway inflammation. Methods Mice were sensitized and challenged by house dust mite (HDM), then exposed to polyinosinic-polycytidylic acid (poly(I:C)) as a model of asthma complicated with viral infection. Mice were administered with EM900. Airway inflammation was assessed from inflammatory cells in bronchoalveolar lavage fluid (BALF) and cytokines in lung tissues. Lung interstitial macrophages were counted by flow cytometry. Cytokine production, phosphorylation of NF-κB, and p38 in macrophages were examined by ELISA and western blotting. Results Counts of cells in BALF and concentrations of IL-13, IL-5, RANTES, IL-17A, and MIP-2 were significantly decreased by EM900 compared to those without EM900. Percentages of lung interstitial macrophages were significantly decreased with EM900. Concentrations of IL-6, RANTES, and MIP-2 induced by HDM and poly(I:C) were significantly suppressed by EM900 through the suppression of NF-κB and p38 phosphorylation in macrophages. Conclusions HDM and poly(I:C)-induced airway inflammation is attenuated by EM900 with the inhibition of lung interstitial macrophages. Clinical use of EM900 is expected, because EM900 has inhibitory effects against airway inflammation without inducing bacterial drug resistance.

scholarly journals Anti-Inflammatory, Immunomodulatory, and Heme Oxygenase-1 Inhibitory Activities of Ravan Napas, a Formulation of Uighur Traditional Medicine, in a Rat Model of Allergic Asthma

2011 ◽  
Vol 2011 ◽  
pp. 1-13 ◽  
Author(s):  
Sajida Abdureyim ◽  
Nurmuhammat Amat ◽  
Anwar Umar ◽  
Halmurat Upur ◽  
Benedicte Berke ◽  
...  
Keyword(s):  
Allergic Asthma ◽  
Bronchoalveolar Lavage Fluid ◽  
Histological Analysis ◽  
Inflammatory Cells ◽  
Lavage Fluid ◽  
Heme Oxygenase 1 ◽  
Asthma Model ◽  
Traditional Uighur Medicine ◽  
Anti Inflammatory ◽  
Marked Suppression

Ravan Napas(RN) is a traditional formula used to treat pulmonary symptoms and diseases such as coughing, breathing difficulty, and asthma in traditional Uighur medicine. The purpose of this study was to investigate the anti-inflammatory, and immuno-modulatory activity of RN in a well-characterized animal model of allergic asthma. Rats were sensitized with intraperitoneal (ip) ovalbumin (OVA) and alum, and then challenged with OVA aerosols. The asthma model rats were treated with RN; saline- and dexamethasone- (DXM-) treated rats served as normal and model controls. The bronchoalveolar lavage fluid (BALF) cellular differential and the concentrations of sICAM-1, IL-4, IL-5, TNF-α, INF-γ, and IgE in serum were measured. Lung sections underwent histological analysis. The immunohistochemistry S-P method was used to measure the expression of ICAM-1 and HO-1 in the lung. RN significantly reduced the number of inflammatory cells in BALF and lung tissues, decreased sICAM-1, IL-4, IL-5, TNF-α, and IgE in serum, and increased serum INF-γ. There was a marked suppression of ICAM-1 and HO-1 expression in the lung. Our results suggest that RN may have an anti-inflammatory and immuneregulatory effect on allergic bronchial asthma by modulating the balance between Th1/Th2 cytokines.

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