Inhibition of allergic airway inflammation through the blockage of NF-κB activation by ellagic acid in an ovalbumin-induced mouse asthma model

2014 ◽  
Vol 5 (9) ◽  
pp. 2106 ◽  
Author(s):  
Ershun Zhou ◽  
Yunhe Fu ◽  
Zhengkai Wei ◽  
Zhengtao Yang
Keyword(s):  
Airway Inflammation ◽  
Ellagic Acid ◽  
Allergic Airway Inflammation ◽  
Asthma Model

Activation of angiotensin-converting enzyme 2 (ACE2) attenuates allergic airway inflammation in rat asthma model

2016 ◽  
Vol 306 ◽  
pp. 17-26 ◽  
Author(s):  
Vaibhav Shrirang Dhawale ◽  
Venkateswara Rao Amara ◽  
Pinakin Arun Karpe ◽  
Vajir Malek ◽  
Deep Patel ◽  
...  
Keyword(s):  
Angiotensin Converting Enzyme ◽  
Airway Inflammation ◽  
Allergic Airway Inflammation ◽  
Converting Enzyme ◽  
Angiotensin Converting Enzyme 2 ◽  
Asthma Model

scholarly journals Schizophyllum commune induces IL-17-mediated neutrophilic airway inflammation in OVA-induced asthma model mice

2019 ◽  
Vol 9 (1) ◽  
Author(s):  
Jun Hanashiro ◽  
Yasunori Muraosa ◽  
Takahito Toyotome ◽  
Koichi Hirose ◽  
Akira Watanabe ◽  
...  
Keyword(s):  
Airway Inflammation ◽  
Asthma Exacerbation ◽  
Schizophyllum Commune ◽  
Allergic Airway Inflammation ◽  
Asthma Severity ◽  
Outdoor Air ◽  
Intratracheal Administration ◽  
Basidiomycetous Fungus ◽  
Asthma Model ◽  
Indoor And Outdoor

AbstractSchizophyllum commune is a ubiquitous basidiomycetous fungus typically found across the world, which has been detected in indoor and outdoor air. Some studies indicated that sensitization to S. commune is correlated with asthma severity in patients. Patients with chronic severe or acute fatal asthma have neutrophil-dominant airway inflammation. We hypothesized that S. commune can exacerbate asthma. To test this hypothesis, we evaluated the direct immunomodulatory activities of S. commune in allergic airway inflammation induced by non-fungal sensitization. Ovalbumin (OVA)-induced asthma model mice were generated using wild-type (WT) and Il-17a−/−Il-17f−/− mice that were intratracheally exposed to S. commune, then immune responses in the lungs were assessed after 24 h. Intratracheal administration of S. commune in OVA-induced asthma model mice enhanced neutrophilic airway inflammation, increased the mRNA expression of CXCL1 and CXCL2 in the lungs, and provoked IL-17A, and IL-17F production in BAL fluid. In addition, neutrophilic airway inflammation was significantly inhibited in Il-17a−/−Il-17f−/− mice compared with those found in WT mice. We demonstrated that S. commune induces neutrophilic airway inflammation in OVA-induced asthma model mice, and IL-17A and IL-17F had central roles in this activity. As S. commune inhabits the general environment, including indoor and outdoor air, our results suggested that S. commune is a causative agent of asthma exacerbation. This study has provided clues regarding the mechanisms behind fungi and asthma exacerbation.

scholarly journals MicroRNA-21 Promotes Allergic Airway Inflammation and AHR and Inhibits Mesenchymal Stem Cell Migration in Cockroach Allergen Induced Asthma Model

2021 ◽  
Author(s):  
Tianli Cheng ◽  
jianfu heng ◽  
Quanhui Mei ◽  
Lijun Chen ◽  
Feng Zeng
Keyword(s):  
Mouse Model ◽  
Airway Inflammation ◽  
Allergic Airway Inflammation ◽  
Airway Hyperreactivity ◽  
Negative Regulator ◽  
Mouse Bone Marrow ◽  
Asthma Model ◽  
Gene Assay

Abstract BackgroundMesenchymal stem cells (MSCs) have been used to treat asthma in a mouse model. However, the efficacy and mechanism of MSCs are not elucidated. MicroRNAs (miRNAs) play a key rolein asthma and related to the aim of this study was to illustrate the role of miR21 and its influence on MSC migration in asthma model. MethodsA mouse model of asthma was established using cockroach extract (CRE), and miR-21 expression was examined. A miR-21 lentivirus construct was used to investigate the role of miR-21 in vivo and in vitro in mouse bone marrow-derived (BM-) MSCs. A TOPFlash reporter gene assay was used to study the signaling downstream of miR-21. IL-4, IL-5, IL-13, IgE, and IgG1 levels in bronchoalveolar lavage fluids were determined by enzyme-linked immunosorbent assays.ResultsMiR-21 was upregulated in CRE-induced asthmatic mice. MiR-21 promoted allergic airway inflammation and airway hyperreactivity by inhibiting BM-MSC migration. β-Catenin was found to act downstream of miR-21 as a negative regulator of miR-21. Rescue experiments verified that miR-21 inhibited BM-MSC migration by suppressing Wnt/β-catenin signaling.ConclusionMiR-21 promotes allergic airway inflammation and AHR and inhibits BM-MSC migration through Wnt/β-catenin signaling, which may serve as an effective therapeutic target for asthma.

scholarly journals Artepillin C Reduces Allergic Airway Inflammation by Induction of Monocytic Myeloid-Derived Suppressor Cells

Pharmaceutics ◽  
2021 ◽  
Vol 13 (11) ◽  
pp. 1763
Author(s):  
Núbia Sabrina Martins ◽  
Thais Fernanda de Campos Fraga-Silva ◽  
Giseli Furlan Correa ◽  
Mèdéton Mahoussi Michaël Boko ◽  
Leandra Naira Zambelli Ramalho ◽  
...  
Keyword(s):  
Airway Inflammation ◽  
Allergic Asthma ◽  
Allergic Airway Inflammation ◽  
Suppressor Cells ◽  
Treg Cells ◽  
Transfer Model ◽  
Myeloid Derived Suppressor Cells ◽  
Asthma Model ◽  
Artepillin C ◽  
Anti Inflammatory

Propolis is a natural product produced by bees that is primarily used in complementary and alternative medicine and has anti-inflammatory, antibacterial, antiviral, and antitumoral biological properties. Some studies have reported the beneficial effects of propolis in models of allergic asthma. In a previous study, our group showed that green propolis treatment reduced airway inflammation and mucus secretion in an ovalbumin (OVA)-induced asthma model and resulted in increased regulatory T cells (Treg) and polymorphonuclear myeloid-derived suppressor cells (PMN-MDSC) frequencies in the lungs, two leukocyte populations that have immunosuppressive functions. In this study, we evaluated the anti-inflammatory effects of artepillin C (ArtC), the major compound of green propolis, in the context of allergic airway inflammation. Our results show that ArtC induces in vitro differentiation of Treg cells and monocytic MDSC (M-MDSC). Furthermore, in an OVA-induced asthma model, ArtC treatment reduced pulmonary inflammation, eosinophil influx to the airways, mucus and IL-5 secretion along with increased frequency of M-MDSC, but not Treg cells, in the lungs. Using an adoptive transfer model, we confirmed that the effect of ArtC in the reduction in airway inflammation was dependent on M-MDSC. Altogether, our data show that ArtC exhibits an anti-inflammatory effect and might be an adjuvant therapy for allergic asthma.

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