Inhaled Carbenoxolone Prevents Allergic Airway Inflammation and Airway Hyperreactivity in a Mouse Model of Asthma

2008 ◽  
Vol 149 (1) ◽  
pp. 38-46 ◽  
Author(s):  
Arjun Ram ◽  
Shashi Kant Singh ◽  
Vijay Pal Singh ◽  
Sarvesh Kumar ◽  
Balaram Ghosh
Keyword(s):  
Mouse Model ◽  
Airway Inflammation ◽  
Allergic Airway Inflammation ◽  
Airway Hyperreactivity

scholarly journals Proteomic Analysis of Anti-inflammatory Effects of a Kampo (Japanese Herbal) Medicine “Shoseiryuto (Xiao-Qing-Long-Tang)” on Airway Inflammation in a Mouse Model

2011 ◽  
Vol 2011 ◽  
pp. 1-13 ◽  
Author(s):  
Takayuki Nagai ◽  
Marino Nakao ◽  
Yuliko Shimizu ◽  
Yoshio Kodera ◽  
Masamichi Oh-Ishi ◽  
...  
Keyword(s):  
Herbal Medicine ◽  
Mouse Model ◽  
Airway Inflammation ◽  
Bronchial Asthma ◽  
Antibody Titer ◽  
Lung Tissue ◽  
Proteomic Analysis ◽  
Allergic Airway Inflammation ◽  
Airway Hyperreactivity ◽  
Japanese Herbal Medicine

Effects of a Kampo (Japanese herbal) medicine “shoseiryuto (SST, xiao-qing-long-tang in Chinese)”, which has been used for the treatment of allergic bronchial asthma clinically, were examined on ovalbumin (OVA)-sensitized allergic airway inflammation model (i.e., bronchial asthma) in a mouse. When SST was orally administered at 0.5 g kg−1 day−1from day 1 to 6 after OVA inhalation, SST reduced the inflammation in lung tissue, the number of eosinophils and the OVA-specific immunoglobulin E (IgE) antibody titer in bronchoalveolar lavage (BAL) fluids at 7 days after the OVA inhalation. SST also reduced the airway hyperreactivity at 6 days after the OVA inhalation. Proteomic analysis with the agarose two-dimensional electrophoresis showed that the expression of spectrin α2 was reduced in the lung tissue of OVA-sensitized mice and SST recovered the expression. Western blot and immunohistochemical analyses of lung tissue also confirmed this result. When prednisolone was orally administered at 3 mg kg−1 day−1from day 1 to 6 after OVA inhalation, the inflammation in lung tissue, the number of eosinophils in BAL fluids and airway hyperreactivity were reduced in the OVA-sensitized mice. However, prednisolone did not reduce the OVA-specific IgE antibody titer in BAL fluids and did not recover the expression of spectrin α2 in lung tissue. These results suggest that at least a part of action mechanism of SST against OVA-sensitized allergic airway inflammation in a mouse model is different from that of prednisolone.

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 Resolved Influenza A Virus Infection Has Extended Effects on Lung Homeostasis and Attenuates Allergic Airway Inflammation in a Mouse Model

2020 ◽  
Vol 8 (12) ◽  
pp. 1878
Author(s):  
Qingyu Wu ◽  
Ilka Jorde ◽  
Olivia Kershaw ◽  
Andreas Jeron ◽  
Dunja Bruder ◽  
...  
Keyword(s):  
Mouse Model ◽  
Airway Inflammation ◽  
Influenza A Virus ◽  
Influenza A ◽  
Inflammatory Responses ◽  
Morphological Changes ◽  
Acute Infection ◽  
Allergic Airway Inflammation ◽  
Airway Hyperreactivity ◽  
Sublethal Dose

Allergic airway inflammation (AAI) involves T helper cell type 2 (Th2) and pro-inflammatory responses to aeroallergens and many predisposing factors remain elusive. Influenza A virus (IAV) is a major human pathogen that causes acute respiratory infections and induces specific immune responses essential for viral clearance and resolution of the infection. Beyond acute infection, IAV has been shown to persistently affect lung homeostasis and respiratory immunity. Here we asked how resolved IAV infection affects subsequently induced AAI. Mice infected with a sublethal dose of IAV were sensitized and challenged in an ovalbumin mediated mouse model for AAI after resolution of the acute viral infection. Histological changes, respiratory leukocytes, cytokines and airway hyperreactivity were analyzed in resolved IAV infection alone and in AAI with and without previous IAV infection. More than five weeks after infection, we detected persistent pneumonia with increased activated CD4+ and CD8+ lymphocytes as well as dendritic cells and MHCII expressing macrophages in the lung. Resolved IAV infection significantly affected subsequently induced AAI on different levels including morphological changes, respiratory leukocytes and lymphocytes as well as the pro-inflammatory cytokine responses, which was clearly diminished. We conclude that IAV has exceptional persisting effects on respiratory immunity with substantial consequences for subsequently induced AAI.

Airway Hyperreactivity Is Associated with Specific Leukocyte Subset Infiltration in a Mouse Model of Allergic Airway Inflammation

Pathobiology ◽  
1996 ◽  
Vol 64 (6) ◽  
pp. 308-313 ◽  
Author(s):  
Nicholas W. Lukacs ◽  
Wayne J.E. Lamm ◽  
Robert M. Strieter ◽  
Richard K. Albert
Keyword(s):  
Mouse Model ◽  
Airway Inflammation ◽  
Allergic Airway Inflammation ◽  
Airway Hyperreactivity ◽  
Leukocyte Subset

OVA-Induced Allergic Airway Inflammation Mouse Model

2018 ◽  
pp. 297-301 ◽  
Author(s):  
Mateus Casaro ◽  
Vanessa R. Souza ◽  
Fernando A. Oliveira ◽  
Caroline M. Ferreira
Keyword(s):  
Mouse Model ◽  
Airway Inflammation ◽  
Allergic Airway Inflammation

scholarly journals Allergen-Specific Treg Cells Upregulated by Lung-Stage S. japonicum Infection Alleviates Allergic Airway Inflammation

2021 ◽  
Vol 9 ◽  
Author(s):  
Zhidan Li ◽  
Wei Zhang ◽  
Fang Luo ◽  
Jian Li ◽  
Wenbin Yang ◽  
...  
Keyword(s):  
Mouse Model ◽  
Protective Effect ◽  
Airway Inflammation ◽  
Lung Tissue ◽  
Immunoglobulin E ◽  
Allergic Airway Inflammation ◽  
Treg Cells ◽  
Protective Effects ◽  
Novel Therapy ◽  
Allergen Sensitization

Schistosoma japonicum infection showed protective effects against allergic airway inflammation (AAI). However, controversial findings exist especially regarding the timing of the helminth infection and the underlying mechanisms. Most previous studies focused on understanding the preventive effect of S. japonicum infection on asthma (infection before allergen sensitization), whereas the protective effects of S. japonicum infection (allergen sensitization before infection) on asthma were rarely investigated. In this study, we investigated the protective effects of S. japonicum infection on AAI using a mouse model of OVA-induced asthma. To explore how the timing of S. japonicum infection influences its protective effect, the mice were percutaneously infected with cercaria of S. japonicum at either 1 day (infection at lung-stage during AAI) or 14 days before ovalbumin (OVA) challenge (infection at post–lung-stage during AAI). We found that lung-stage S. japonicum infection significantly ameliorated OVA-induced AAI, whereas post–lung-stage infection did not. Mechanistically, lung-stage S. japonicum infection significantly upregulated the frequency of regulatory T cells (Treg cells), especially OVA-specific Treg cells, in lung tissue, which negatively correlated with the level of OVA-specific immunoglobulin E (IgE). Depletion of Treg cells in vivo partially counteracted the protective effect of lung-stage S. japonicum infection on asthma. Furthermore, transcriptomic analysis of lung tissue showed that lung-stage S. japonicum infection during AAI shaped the microenvironment to favor Treg induction. In conclusion, our data showed that lung-stage S. japonicum infection could relieve OVA-induced asthma in a mouse model. The protective effect was mediated by the upregulated OVA-specific Treg cells, which suppressed IgE production. Our results may facilitate the discovery of a novel therapy for AAI.

Blocking ATP releasing channels prevents high extracellular ATP levels and airway hyperreactivity in an asthmatic mouse model

2021 ◽  
Author(s):  
Llilian Arzola Martínez ◽  
Rebeca Benavente ◽  
Génesis Vega ◽  
Mariana Ríos ◽  
Wendy Fonseca ◽  
...  
Keyword(s):  
Mouse Model ◽  
Airway Inflammation ◽  
Airway Epithelium ◽  
Atp Release ◽  
Specific Inhibitor ◽  
Extracellular Atp ◽  
Airway Hyperreactivity ◽  
Luciferase Assay ◽  
Asthmatic Patients ◽  
Allergic Mouse

Allergic asthma is a chronic airway inflammatory response to different triggers like inhaled allergens. Excessive ATP in fluids from asthmatic patients is considered an inflammatory signal and an important autocrine/paracrine modulator of airway physiology. Here we investigated the deleterious effect of increased extracellular ATP (eATP) concentration on the mucociliary clearance (MCC) effectiveness and determined the role of ATP releasing channels during airway inflammation in an ovalbumin (OVA)-sensitized mouse model. Our allergic mouse model exhibited high levels of eATP measured in the tracheal fluid with a luciferin-luciferase assay and reduced MCC velocity determined by microspheres tracking in the trachea ex vivo. Addition of ATP had a dual effect on MCC, where lower ATP concentration (µM) increased microspheres velocity, while higher concentration (mM) transiently stopped microspheres movement. Also, an augmented ethidium bromide uptake by the allergic tracheal airway epithelium suggests an increase in ATP release channel functionality during inflammatory conditions. The use of carbenoxolone, a non-specific inhibitor of connexin and pannexin1channels reduced the eATP concentration in the allergic mouse tracheal fluid and dye uptake by the airway epithelium, providing evidence that these ATP release channels are facilitating the net flux of ATP to the lumen during airway inflammation. However, only the specific inhibition of pannexin1 with 10Panx peptide significantly reduced eATP in bronchoalveolar lavage and decreased airway hyperresponsiveness in OVA-allergic mouse model. These data provide evidence that blocking eATP may be a pharmacological alternative to be explored in rescue therapy during episodes of airflow restriction in asthmatic patients.

scholarly journals Ascaris lumbricoides Cystatin Prevents Development of Allergic Airway Inflammation in a Mouse Model

2019 ◽  
Vol 10 ◽  
Author(s):  
Sandra Coronado ◽  
Josefina Zakzuk ◽  
Ronald Regino ◽  
Velky Ahumada ◽  
Ines Benedetti ◽  
...  
Keyword(s):  
Mouse Model ◽  
Airway Inflammation ◽  
Ascaris Lumbricoides ◽  
Allergic Airway Inflammation
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