scholarly journals LncRNA-AK149641 associated with airway inflammation in an OVA-induced asthma mouse model

2020 ◽  
Vol 52 (5) ◽  
pp. 355-365
Author(s):  
Jie Zhang ◽  
Yao Zhou ◽  
Haiyan Gu ◽  
Jiamin Zhang ◽  
Heng Tang ◽  
...  
Keyword(s):  
Mouse Model ◽  
Airway Inflammation ◽  
Lung Tissue ◽  
Inflammatory Cells ◽  
Differentially Expressed ◽  
Necrosis Factor Alpha ◽  
Adeno Associated Virus ◽  
Gene Microarray Analysis ◽  
And Control ◽  
Asthma Mouse Model

Abstract Asthma is defined as a heterogeneous disease, usually characterized by chronic airway inflammation. Long noncoding RNAs (lncRNAs) play important roles in various biological processes. To know more about the relationships between lncRNAs and asthma, gene microarray analysis was performed to screen differentially expressed lncRNAs between the lung tissue of ovalbumin (OVA) mice and control mice. Further studies showed that downregulating differentially expressed lncRNA-AK149641 by adeno-associated virus 6 (AAV6) in OVA mice inhibited airway inflammation, with improved airway compliance and resistance, diminished infiltration of inflammatory cells, as well as less secretions of mucus, tumor necrosis factor alpha (TNF-α) and interleukin-6 (IL-6). Moreover, the activity of nuclear factor-kappa B (NF-κB) in the lung tissue was reduced after downregulating lncRNA-AK149641. In conclusion, we proposed that downregulation of lncRNA-AK149641 attenuated the airway inflammatory response in an OVA-induced asthma mouse model, probably in association with modulation of the NF-κB signaling pathway.

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.

CRM197-Coupled Der p 2 Peptides Suppress Allergic Airway Inflammation in a Der p 2-Induced Asthma Mouse Model

2019 ◽  
Vol 180 (3) ◽  
pp. 173-181
Author(s):  
Cong Wang ◽  
Luo Wang ◽  
Ban-Cheng Chen ◽  
Hao Yu ◽  
Lu Li ◽  
...  
Keyword(s):  
Mouse Model ◽  
Airway Inflammation ◽  
Allergic Airway Inflammation ◽  
Der P 2 ◽  
Asthma Mouse Model

scholarly journals Loki zupa (Luooukezupa) decoction reduced airway inflammation in an OVA-induced asthma mouse model

2016 ◽  
Vol 11 (1) ◽  
Author(s):  
Ying Wei ◽  
Muhammadjan Abduwaki ◽  
Mihui Li ◽  
Qingli Luo ◽  
Jing Sun ◽  
...  
Keyword(s):  
Mouse Model ◽  
Airway Inflammation ◽  
Asthma Mouse Model

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 Allergen specific Treg upregulated by lung-stage schistosome infection alleviates allergic airway inflammation via inhibiting IgE secretion

2020 ◽  
Author(s):  
Zhi dan Li ◽  
Wei Zhang ◽  
fang Luo ◽  
jian Li ◽  
Wen bin Yang ◽  
...  
Keyword(s):  
Mouse Model ◽  
Airway Inflammation ◽  
Therapeutic Effect ◽  
Lung Tissue ◽  
Allergic Airway Inflammation ◽  
Therapeutic Effects ◽  
Protective Effects ◽  
Schistosome Infection ◽  
Allergen Sensitization ◽  
Asthma Attack

Schistosome infection showed protective effects against allergic airway inflammation (AAI). However,controversial findings exist especially regarding the timing of helminth infection and the underlying mechanisms. Moreover, most previous studies focused on understanding the preventive effect of schistosome infection on asthma (infection before allergen sensitization), while its therapeutic effects (infection after allergen sensitization) were rarely investigated. In this study, we investigated the therapeutic effects of schistosome infection on AAI using a mouse model of OVA induced asthma. To explore how the timing of schistosome infection influences its therapeutic effect, the mice were percutaneously infected with cercaria of Schistosoma japonicum at either 1 day before OVA induced asthma attack (infection at lung-stage during AAI) or 14 days before OVA induced asthma attack (infection at post lung-stage during AAI). We found that lung-stage schistosome infection significantly ameliorated OVA-induced AAI, whereas post lung-stage infection showed no therapeutic effect. Mechanistically, the lung-stage schistosome infection significantly upregulated the frequency of Treg, especially OVA specific Treg, in lung tissue, which negatively correlated with the level of OVA specific IgE. Depletion of Treg in vivo counteracted the therapeutic effect. Furthermore, transcriptomic analysis of lung tissue showed that lung-stage schistosome infection during AAI shaped the microenvironment to favor Treg induction. In conclusion, our data showed that lung-stage schistosome infection could relieve OVA induced asthma in a mouse model. The therapeutic effect was mediated by the upregulated OVA specific Treg which suppressed IgE production and Th2 cytokine secretion. Our results may facilitate the discovery of a new therapy for AAI.

scholarly journals Lactobacillus gasseri suppresses Th17 pro-inflammatory response and attenuates allergen-induced airway inflammation in a mouse model of allergic asthma

2011 ◽  
Vol 108 (1) ◽  
pp. 130-139 ◽  
Author(s):  
Ren-Long Jan ◽  
Kung-Chih Yeh ◽  
Miao-Hsi Hsieh ◽  
Yen-Lin Lin ◽  
Hui-Fang Kao ◽  
...  
Keyword(s):  
Mouse Model ◽  
Oral Administration ◽  
Airway Inflammation ◽  
Allergic Asthma ◽  
Transforming Growth Factor ◽  
Allergen Challenge ◽  
Inflammatory Cells ◽  
Airway Responsiveness ◽  
High Dose ◽  
Lactobacillus Gasseri

Probiotics are normal inhabitants of the gastrointestinal tract of man and are widely considered to exert a number of beneficial effects in many diseases. But the mechanism by which they modulate the immune system is poorly understood. The present study was planned to explore the anti-allergic effect of Lactobacillus gasseri on a mouse model of allergic asthma. Dermatophoides pteronyssinus (Der p) sensitised and challenged BALB/c mice were orally administered via oral administration with three different doses of L. gasseri (low, 1 × 106 colony-forming units (CFU); medium, 2 × 106 CFU; high, 4 × 106 CFU), in 700 μl of PBS daily, starting from 2 weeks before Der p sensitisation for 4 weeks. After the allergen challenge, airway responsiveness to methacholine, influx of inflammatory cells to the lung, and cytokine levels in bronchoalveolar lavage (BAL) fluids and splenocytes culture were assessed. Our results showed that oral administration of a high dose of L. gasseri (4 × 106 CFU) decreased airway responsiveness to methacholine, attenuated the influx of inflammatory cells to the airways and reduced the levels of TNF-α, thymus and activation-regulated chemokine (TARC) and IL-17A in BAL fluids of Der p-sensitised and -challenged mice. Moreover, L. gasseri decreased IL-17A production in transforming growth factor-α and IL-6 stimulated splenocytes and cell numbers of IL-17 producing alveolar macrophages in L. gasseri-treated mice as compared to non-treated, Der p-sensitised and -challenged mice. In conclusion, oral administration with L. gasseri can attenuate major characteristics of allergen-induced airway inflammation and IL-17 pro-inflammatory immune response in a mouse model of allergic asthma, which may have clinical implication in the preventive or therapeutic potential in allergic asthma.

Dendritic cells inversely regulate airway inflammation in cigarette smoke-exposed mice

2016 ◽  
Vol 310 (1) ◽  
pp. L95-L102 ◽  
Author(s):  
Masoumeh Ezzati Givi ◽  
Peyman Akbari ◽  
Louis Boon ◽  
Vladimir S. Puzovic ◽  
Gillina F. G. Bezemer ◽  
...  
Keyword(s):  
Dendritic Cells ◽  
Airway Inflammation ◽  
Cigarette Smoke ◽  
Lung Tissue ◽  
Inflammatory Cells ◽  
Chronic Obstructive ◽  
Obstructive Pulmonary Disease ◽  
Crucial Feature ◽  
Plasmacytoid Dcs ◽  
Lung Tissue Damage

The recruitment and activation of inflammatory cells into the respiratory system is considered a crucial feature in the pathophysiology of chronic obstructive pulmonary disease (COPD). Because dendritic cells (DCs) have a pivotal role in the onset and regulation of immune responses, we investigated the effect of modulating DC subsets on airway inflammation by acute cigarette smoke (CS) exposure. CS-exposed mice (5 days) were treated with fms-like tyrosine kinase 3 ligand (Flt3L) and 120g8 antibody to increase total DC numbers and deplete plasmacytoid DCs (pDCs), respectively. Flt3L treatment decreased the number of inflammatory cells in the bronchoalveolar lavage (BALF) of the smoke-exposed mice and increased these in lung tissue. DC modulation reduced IL-17 and increased IL-10 levels, which may be responsible for the suppression of the BALF cells. Furthermore, depletion of pDCs led to increased infiltration of alveolar macrophages while restricting the presence of CD103+ DCs. This study suggests that DC subsets may differentially and compartment-dependent influence the inflammation induced by CS. pDC may play a role in preventing the pathogenesis of CS by inhibiting the alveolar macrophage migration to lung and increasing CD103+ DCs at inflammatory sites to avoid extensive lung tissue damage.

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