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.

scholarly journals Impacts of allergic airway inflammation on lung pathology in a mouse model of influenza A virus infection

PLoS ONE ◽  
2017 ◽  
Vol 12 (2) ◽  
pp. e0173008 ◽  
Author(s):  
Akira Kawaguchi ◽  
Tadaki Suzuki ◽  
Yuki Ohara ◽  
Kenta Takahashi ◽  
Yuko Sato ◽  
...  
Keyword(s):  
Virus Infection ◽  
Mouse Model ◽  
Airway Inflammation ◽  
Influenza A Virus ◽  
Influenza A ◽  
Allergic Airway Inflammation ◽  
Lung Pathology ◽  
Influenza A Virus Infection

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 CD103 integrin identifies a high IL-10-producing FoxP3 + regulatory T cell population suppressing allergic airway inflammation

2021 ◽  
Author(s):  
Sofia Tagkareli ◽  
Maria Salagianni ◽  
Ioanna Galani ◽  
Maria Manioudaki ◽  
Eleftherios Pavlos ◽  
...  
Keyword(s):  
T Cell ◽  
Mouse Model ◽  
Airway Inflammation ◽  
Cell Population ◽  
Regulatory T Cell ◽  
Inflammatory Responses ◽  
Allergic Inflammation ◽  
Allergic Airway Inflammation ◽  
Treg Cells ◽  
Dependent Manner

Background: Although FoxP3 regulatory T (Treg) cells constitute a highly heterogeneous population, with different regulatory potential depending on the disease context, distinct subsets or phenotypes remain poorly defined. This hampers the development of immunotherapy for allergic and autoimmune disorders. Objective: This study aimed at characterizing distinct FoxP3 Treg subpopulations involved in the suppression of Th2-mediated allergic inflammation in the lung. Methods: We used an established mouse model of allergic airway disease based on ovalbumin sensitization and challenge to analyze FoxP3 Tregs during the induction and resolution of inflammation, and identify markers that distinguish their most suppressive phenotypes. We also developed a new knock-in mouse model ( Foxp3Cd103) enabling the specific ablation of CD103 FoxP3 Tregs for functional studies. Results: We found that during resolution of allergic airway inflammation in mice >50% of FoxP3 Treg cells expressed the integrin CD103 which marks FoxP3 Treg cells of high IL-10 production, increased expression of immunoregulatory molecules such as KLRG1, ICOS and CD127, and enhanced suppressive capacity for Th2-mediated inflammatory responses. CD103 FoxP3 Tregs were essential for keeping allergic inflammation under control as their specific depletion in Foxp3Cd103 mice lead to severe alveocapillary damage, eosinophilic pneumonia, and markedly reduced lifespan of the animals. Conversely, adoptive transfer of CD103 FoxP3 Tregs effectively treated disease, attenuating Th2 responses and allergic inflammation in an IL-10-dependent manner. Conclusion: Our study identifies a novel regulatory T cell population, defined by CD103 expression, programmed to prevent exuberant type 2 inflammation and keep homeostasis in the respiratory tract under control. This has important therapeutic implications.

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

scholarly journals CD103 integrin identifies a high IL-10-producing FoxP3+ regulatory T cell population suppressing allergic airway inflammation

2021 ◽  
Author(s):  
Sofia Tagkareli ◽  
Maria Salagianni ◽  
Ioanna Galani ◽  
Maria Manioudaki ◽  
Eleftherios Pavlos ◽  
...  
Keyword(s):  
T Cell ◽  
Mouse Model ◽  
Airway Inflammation ◽  
Cell Population ◽  
Regulatory T Cell ◽  
Inflammatory Responses ◽  
Allergic Inflammation ◽  
Allergic Airway Inflammation ◽  
Treg Cells ◽  
Dependent Manner

Background: Although FoxP3+ regulatory T (Treg) cells constitute a highly heterogeneous population, with different regulatory potential depending on the context, distinct subsets or phenotypes remain poorly defined. This hampers the development of immunotherapy for allergic and autoimmune disorders. This study aimed at characterizing distinct FoxP3+ Treg subpopulations involved in the suppression of Th2-mediated allergic inflammation in the lung. Methods: We used an established mouse model of allergic airway disease based on ovalbumin sensitization and challenge to analyze FoxP3+ Tregs during the induction and resolution of inflammation, and identify markers that distinguish their most suppressive phenotypes. We also developed a new knock-in mouse model (Foxp3creCd103dtr) enabling the specific ablation of CD103+FoxP3+ Tregs for functional studies. Results: We found that during resolution of allergic airway inflammation in mice >50% of FoxP3+ Treg cells expressed the integrin CD103 which marks FoxP3+ Treg cells of high IL-10 production, increased expression of immunoregulatory molecules such as KLRG1, ICOS and CD127, and enhanced suppressive capacity for Th2-mediated inflammatory responses. CD103+FoxP3+ Tregs were essential for keeping allergic inflammation under control as their specific depletion in Foxp3creCd103dtr mice lead to severe alveocapillary damage and eosinophilic pneumonia, markedly reducing the lifespan of the experimental animals. Conversely, adoptive transfer of CD103+FoxP3+ Tregs effectively treated disease, attenuating Th2 responses and allergic inflammation in an IL-10-dependent manner. Conclusion: Our study identifies a novel regulatory T cell population, defined by CD103 expression, programmed to prevent exuberant type 2 inflammation and keep homeostasis in the respiratory tract under control. This has important therapeutic implications.

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