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.

Effects of Radix Platycodonis Polysaccharide on Expressions of IFN-γ, IL-4 and IL-5 in the Bronchoalveolar Lavage Fluid and Nf-κВ in the Lung Tissue of Asthmatic Rats

2013 ◽  
Vol 750-752 ◽  
pp. 1549-1554
Author(s):  
Xiao Dong Huang ◽  
Xing Yu Zhao ◽  
Yan Chun Wang ◽  
Jian Ying
Keyword(s):  
Lavage Fluid ◽  
Enzyme Linked Immunosorbent Assay ◽  
Control Group ◽  
High Dose ◽  
Model Group ◽  
Blank Control Group ◽  
Asthma Model ◽  
Ifn Γ ◽  
Group 1

Objective: To investigate the effect of Radix playtycodoni polysaccharide (RPPS) on rats with ovalbumin-induced asthma and its mechanisms. Methods: 48 Wistar rats were randomly divided into blank control group, asthma model group, dexamethasone control group (1 mg / kg), and high-dose RPPS group (40 mg / kg), moderate-dose RPPS group (20 mg / kg) and low-dose RPPS group (10 mg / kg). The ovalbumin sensitization method was used to establish the asthma model in rats. The rats were given it in the atomization administration for two weeks and then were sacrificed. The BALF was collected for the count of eosinophils (EOS); enzyme-linked immunosorbent assay (ELISA) method was employed for the determination of IL-4, IL-5, and IFN-γ levels in BALF; the expression of NF-κВ in the lung tissues was measured by Western blot. Results: Compared with the model group, RPPS could reduce the number of EOS in blood and BALF, increase the content of IFN-γ in BALF, lower IL-4 and IL-5 contents, and down-regulate the expression of NF-κВ protein in rats with asthma. Conclusion: RPPS can inhibit the airway inflammation in asthma, down-regulate the expression level of IL-4 and IL-5, up-regulate the IFN-γ level to regulate the abnormal immune status induced by the imbalance of TH1/TH2 in asthma and inhibit the expression of NF-κВ, which may be one of the mechanisms of its anti-inflammatory activity.

scholarly journals Changes in Pulmonary Function and Parasite Burden in Rats Infected with Strongyloides venezuelensis Concomitant with Induction of Allergic Airway Inflammation

2003 ◽  
Vol 71 (5) ◽  
pp. 2607-2614 ◽  
Author(s):  
Deborah Negrão-Corrêa ◽  
Micheline R. Silveira ◽  
Cynthia M. Borges ◽  
Danielle G. Souza ◽  
Mauro M. Teixeira
Keyword(s):  
Airway Inflammation ◽  
Mutual Influence ◽  
Pulmonary Inflammation ◽  
Allergic Airway Inflammation ◽  
Parasite Burden ◽  
Allergic Diseases ◽  
Lavage Fluid ◽  
Eosinophil Infiltration ◽  
Asthmatic Patients ◽  
Strongyloides Venezuelensis

ABSTRACT The prevalence of allergic diseases such as asthma has increased markedly over the past few decades. To evaluate the possible mutual influence of helminth infection and allergy, the combined effects of experimental allergic airway inflammation and infection with Strongyloides venezuelensis on various parasitological and inflammatory indices were evaluated in the rat. A challenge of immunized rats with aerosolized ovalbumin (OVA) resulted in eosinophilic inflammation that peaked 48 h after the challenge and was accompanied by airway hyperresponsiveness (AHR) to an intravenous acetylcholine challenge. S. venezuelensis infection concomitant with an OVA challenge of immunized rats resulted in prolonged pulmonary inflammation with increased eosinophil infiltration in bronchoalveolar lavage fluid but not in the lung tissue. These rats also showed a significant parasite burden reduction, especially during parasite migration through the lungs. However, the fecundity rates of worms that reached the intestine were similar in allergic and nonallergic animals. Despite airway inflammation, the increased responsiveness of the airways in the experimental asthma model was suppressed during parasite migration through the lungs (2 days). In contrast, parasite-induced AHR was unchanged 5 days after infection in immunized and challenged rats. In conclusion, infection with S. venezuelensis interfered with the onset of AHR following an antigen challenge of immunized rats. The ability of parasites to switch off functional airway responses is therapeutically relevant because we may learn from parasites how to modulate lung function and, hence, the AHR characteristic of asthmatic patients.

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 VIWITHAN: A STANDARDIZED ASHWAGANDHA EXTRACT AMELIORATES OVALBUMININDUCED AIRWAY-INFLAMMATION AND OXIDATIVE STRESS IN MOUSE MODEL

2021 ◽  
pp. 89-93
Author(s):  
VASAVI HS ◽  
SUDEEP HV ◽  
RAMANAIAH ILLURI ◽  
SHYAMPRASAD K
Keyword(s):  
Oxidative Stress ◽  
Airway Inflammation ◽  
Transforming Growth Factor ◽  
Lavage Fluid ◽  
Interleukin 10 ◽  
Transforming Growth Factor Β1 ◽  
Lung Pathology ◽  
Protective Effects ◽  
Lung Weight ◽  
And Oxidative Stress

Objective: Withania somnifera, commonly known as Ashwagandha, Indian ginseng, has been used in Ayurvedic and indigenous medicinal preparations for various disease conditions since long time. In the present study, we investigated the protective effects of Viwithan, a standardized proprietary extract from Ashwagandha roots, against airway-inflammation and oxidative stress modulation in an ovalbumin (OVA)-induced murine model of inflammation. Methods: Allergic asthma was initiated in BALB/c mice by sensitizing with OVA on days 1 and 14, followed by intranasal challenge with OVA on days 27, 28, and 29. Mice were administered Viwithan (200 and 400 mg/kg) by oral gavage before challenge. Then, mice were evaluated for the presence of airway inflammation, production of allergen-specific cytokine response, lung pathology, and oxidative stress modulation. Results: The results showed that treatment with Viwithan attenuated OVA-induced lung inflammation in mice. Viwithan significantly attenuated inflammatory cell infiltration into the bronchoalveolar lavage fluid and markedly reduced the levels of pro-inflammatory cytokines, interleukin-10, and transforming growth factor-β1 in lung tissues. Viwithan treatment considerably reduced the lung weight in OVA-sensitized mice. Viwithan markedly attenuated the OVA-induced generation of reactive oxygen species in lung tissues. Conclusion: Together, these results suggested that Viwithan alleviates OVA-induced airway-inflammation and oxidative stress, highlighting the potential of standardized Ashwagandha extract as a useful therapeutic agent for pulmonary fibrosis management.

Relation of Interleukin-10 in Bronchoalveolar Lavage Fluid and Airway Inflammation in Bronchial Asthma

1999 ◽  
Vol 46 (1) ◽  
pp. 44
Author(s):  
Sook Young Lee ◽  
Hung Gue Youn ◽  
Youn Shin ◽  
Sang Haak Lee ◽  
Seok Chan Kim ◽  
...  
Keyword(s):  
Bronchoalveolar Lavage ◽  
Airway Inflammation ◽  
Bronchial Asthma ◽  
Bronchoalveolar Lavage Fluid ◽  
Lavage Fluid ◽  
Interleukin 10

Salidroside Mitigates Airway Inflammation in Asthmatic Mice via the AMPK/Akt/GSK3β Signaling Pathway

2021 ◽  
pp. 1-11
Author(s):  
Xue Luan ◽  
Chunai Cui ◽  
Jingzhi Jiang ◽  
Chongyang Wang ◽  
Li Li ◽  
...  
Keyword(s):  
Airway Inflammation ◽  
Dose Group ◽  
Bronchial Hyperresponsiveness ◽  
Lavage Fluid ◽  
Inflammatory Factors ◽  
Control Group ◽  
High Dose ◽  
Inflammatory Infiltration ◽  
Ifn Γ

<b><i>Introduction:</i></b> This study aimed to explore the effects and mechanisms of salidroside (SAL) in airway inflammation in asthmatic mice. <b><i>Methods:</i></b> Mice were sensitized with ovalbumin (OVA) to establish an asthma model. They were divided into the control group, OVA group, SAL low-dose group (SAL-L), SAL high-dose group (SAL-H), and dexamethasone (DXM) group. The airway reactivity of the mice was measured, and the total cells, neutrophils, eosinophils, and lymphocytes were counted, respectively. The levels of IL-4, IL-5, IL-13, and IFN-γ in bronchoalveolar lavage fluid (BALF) were detected by ELISA. Immunohistochemistry was used to detect the expression levels of p-AMPK, p-Akt, and p-GSK3β. Western blot was used to detect cytokine levels in lung tissue and p-AMPK, p-Akt, and p-GSK3β levels in LPS-induced 16HBE cells. <b><i>Results:</i></b> The airway hyperresponsiveness of asthmatic mice in the SAL-H group decreased (<i>p</i> &#x3c; 0.05), and the total number of cells, neutrophils, eosinophils, and lymphocytes decreased significantly (<i>p</i> &#x3c; 0.05). In addition, the airways of mice showed airway inflammatory infiltration and goblet cell proliferation, and the corresponding cellular inflammatory factors IL-4, IL-5, and IL-13 were significantly decreased. However, the expression of IFN-γ in BALF and lung tissues was increased (<i>p</i> &#x3c; 0.05). Moreover, after the mice were treated with SAL, the phosphorylation level of AMPK was significantly increased, which further reduced the phosphorylation levels of Akt and GSK3β (<i>p</i> &#x3c; 0.05). Both SAL and AMPK inhibitors exerted effects on LPS-induced 16HBE cells, consistent with in vivo results. <b><i>Conclusion:</i></b> SAL can inhibit bronchial hyperresponsiveness and reduce tracheal inflammation by increasing AMPK phosphorylation and inhibiting Akt and GSK3β signaling pathways.

IL-10 reduces grain dust-induced airway inflammation and airway hyperreactivity

2000 ◽  
Vol 88 (1) ◽  
pp. 173-179 ◽  
Author(s):  
Timothy J. Quinn ◽  
Somer Taylor ◽  
Christine L. Wohlford-Lenane ◽  
David A. Schwartz
Keyword(s):  
Airway Inflammation ◽  
Airway Disease ◽  
Lavage Fluid ◽  
Interleukin 10 ◽  
Airway Hyperreactivity ◽  
Lower Percentage ◽  
Polymorphonuclear Cells ◽  
Inhalation Challenge ◽  
Grain Dust ◽  
Dust Extract

To determine whether interleukin-10 (IL-10) could alter the development of grain dust-induced airway disease, we pretreated mice with either saline or IL-10 intravenously, exposed the mice to an inhalation challenge with corn dust extract (CDE), and measured inflammation and the development of airway hyperreactivity. Pretreatment with IL-10, in comparison to saline, reduced the concentration and percentage of polymorphonuclear cells in the lavage fluid 30 min after the inhalation challenge with CDE ( P < 0.05). In comparison to saline-treated mice, IL-10 did not significantly alter the degree of airway hyperreactivity 30 min after the exposure to CDE. IL-10-treated mice lavaged 18 h after challenge with CDE also exhibited a lower percentage of polymorphonuclear cells in the lavage fluid ( P < 0.05) and had significantly less airway hyperreactivity than did mice pretreated with the saline placebo ( P < 0.05). These findings indicate that exogenous IL-10 is effective in reducing airway inflammation and airway hyperreactivity due to the inhalation of CDE.

Human parainfluenza type 3 virus impairs the efficacy of glucocorticoids to limit allergy-induced pulmonary inflammation in guinea-pigs

2013 ◽  
Vol 125 (10) ◽  
pp. 471-482 ◽  
Author(s):  
William R. Ford ◽  
Alan E. Blair ◽  
Rhys L. Evans ◽  
Elinor John ◽  
Joachim J. Bugert ◽  
...  
Keyword(s):  
Airway Obstruction ◽  
Guinea Pigs ◽  
Inflammatory Cell ◽  
Pulmonary Inflammation ◽  
Late Phase ◽  
Allergen Challenge ◽  
Lavage Fluid ◽  
Whole Body ◽  
Cell Counts ◽  
Type 3

Viral exacerbations of allergen-induced pulmonary inflammation in pre-clinical models reportedly reduce the efficacy of glucocorticoids to limit pulmonary inflammation and airways hyper-responsiveness to inhaled spasmogens. However, exacerbations of airway obstruction induced by allergen challenge have not yet been studied. hPIV-3 (human parainfluenza type 3 virus) inoculation of guinea-pigs increased inflammatory cell counts in BAL (bronchoalveolar lavage) fluid and caused hyper-responsiveness to inhaled histamine. Both responses were abolished by treatment with either dexamethasone (20 mg/kg of body weight, subcutaneous, once a day) or fluticasone propionate (a 0.5 mg/ml solution aerosolized and inhaled over 15 min, twice a day). In ovalbumin-sensitized guinea-pigs, allergen (ovalbumin) challenge caused two phases of airway obstruction [measured as changes in sGaw (specific airways conductance) using whole body plethysmography]: an immediate phase lasting between 4 and 6 h and a late phase at about 7 h. The late phase, airway hyper-responsiveness to histamine and inflammatory cell counts in BAL were all significantly reduced by either glucocorticoid. Inoculation of guinea-pigs sensitized to ovalbumin with hPIV-3 transformed the allergen-induced airway obstruction from two transient phases into a single sustained response lasting up to 12 h. This exacerbated airway obstruction and airway hyper-responsiveness to histamine were unaffected by treatment with either glucocorticoid whereas inflammatory cell counts in BAL were only partially inhibited. Virus- or allergen-induced pulmonary inflammation, individually, are glucocorticoid-sensitive, but in combination generate a phenotype where glucocorticoid efficacy is impaired. This suggests that during respiratory virus infection, glucocorticoids might be less effective in limiting pulmonary inflammation associated with asthma.

Low-dose theophylline restores corticosteroid responsiveness in rats with smoke-induced airway inflammation

2012 ◽  
Vol 90 (7) ◽  
pp. 895-902 ◽  
Author(s):  
Xianwen Sun ◽  
Qingyun Li ◽  
Yi Gong ◽  
Lei Ren ◽  
Huanying Wan ◽  
...  
Keyword(s):  
Airway Inflammation ◽  
Low Dose ◽  
Corticosteroid Treatment ◽  
Lavage Fluid ◽  
Cell Counting ◽  
Chronic Obstructive ◽  
High Dose ◽  
Obstructive Pulmonary Disease ◽  
Histone Deacetylase 2 ◽  
Chemokine Ligand

Patients with chronic obstructive pulmonary disease (COPD) respond poorly to corticosteroids. Histone deacetylase-2 (HDAC-2) plays a pivotal role in many cases of steroid insensitivity. The main aim of this study was to restore the smoking-induced reduction in corticosteroid sensitivity by increasing HDAC-2 activity using low-dose theophylline. Rats were exposed to cigarette smoke (CS) and treated with budesonide and two doses of theophylline. Besides the pathologic examination and cell counting in the bronchoalveolar lavage fluid (BALF), the expression of HDAC-2 and CXC chemokine ligand-8 (CXCL-8) were measured. Airway inflammation induced by CS was demonstrated by pathologic changes of lung tissue and increased level of CXCL-8. CS exposure also markedly decreased HDAC-2 expression. Moreover, a negative correlation was found between HDAC-2 activity and a lung destruction index. The index was restored to control levels with inhaled corticosteroid treatment in combination with a low, not a high, dose of theophylline. These results indicate that low-dose theophylline might provide protection from smoke damage and improve the anti-inflammatory effects of steroids by increasing HDAC-2 activity.

scholarly journals Transtracheal Instillation of Anti-TSLP Antibody Alleviates Airway Inflammation and Airway Hyperresponsiveness in OVA-Induced Asthma Model Mice

2021 ◽  
Author(s):  
Xiaowen Chen ◽  
Xiangfeng Fang ◽  
Jiang Qian ◽  
Jinle Lin ◽  
DongFeng Li ◽  
...  
Keyword(s):  
Airway Inflammation ◽  
Airway Hyperresponsiveness ◽  
Animal Studies ◽  
Histopathological Examination ◽  
Allergic Inflammation ◽  
Inflammatory Cells ◽  
Control Group ◽  
Model Group ◽  
Protein Levels ◽  
Asthma Model

Abstract BackgroundThymic stromal lymphopoietin (TSLP) is a mainly epithelial cell-derived cytokine that may be important in initiating T2 allergic inflammation. Anti-TSLP antibody inhibit allergic inflammation. Previous animal studies have evaluated the anti-allergic efficacy of injecting anti-TSLP antibody intraperitoneally, subcutaneously, or intravenously. However, transtracheal instillation, a less invasive route for anti-TSLP antibody administration, is hitherto unstudied. This study evaluates the efficacy of transtracheally instilling anti-TSLP antibody in inhibiting airway inflammation and hyperresponsiveness in OVA-induced asthma model Balb/c mice.MethodsBalb/c mice were randomly divided into four groups: the control group, the OVA-induced asthma model group, the anti-TSLP mAb treatment group (TSLP mAb group), and the IgG2a mAb control group (IgG2a mAb group). Each group contained nine to eleven mice. Mice in the asthma model group were sensitized with OVA to trigger allergic responses and were treated with transtracheal instillation of normal saline. Mice in the TSLP mAb group received transtracheal instillation of anti-TSLP mAb, while mice in the IgG2a group received transtracheal instillation of IgG2a mAb. Both of these groups were then subjected to OVA challenge. Airway responsiveness was measured as an enhanced pause (Penh) using noninvasive plethysmography. The severity of inflammation was evaluated by histopathological examination using the Underwood assessment of the lung sections. Changes in expression of TSLP, TSLP receptor (TSLPR), T-box transcription factor (T-bet), GATA binding protein 3 (GATA3) and forkhead box protein P3 (Foxp3) were assessed using RT-PCR and immunohistochemical staining. ResultsAirway hyperresponsiveness and infiltration of airway inflammatory cells in the TSLP mAb group were significantly reduced, compared with the OVA and the IgG2a mAb groups. Meanwhile，TSLP, GATA3 mRNA expression and GATA3 protein levels were significantly decreased in the TSLP mAb group, compared with the OVA and the IgG2a mAb groups (P＜0.05）. No significant differences were observed in either T-bet or Foxp3 in the lung section of mRNA and protein expression among these four groups (P＞0.05).ConclusionTranstracheal instillation of anti-TSLP antibody attenuated lung inflammation and airway hyperresponsiveness in OVA-induced asthmatic mice, possibly through downregulation of perivascular and peribronchiolar lymphocytes, neutrophils and GATA3 expression in the airway.

Sign in / Sign up

Export Citation Format

Share Document