scholarly journals IL-6 Deficiency Exacerbates Allergic Asthma and Abrogates the Protective Effect of Allergic Inflammation against Streptococcus pneumoniae Pathogenesis

2020 ◽  
Vol 205 (2) ◽  
pp. 469-479
Author(s):  
Taylor Schmit ◽  
Sumit Ghosh ◽  
Ram Kumar Mathur ◽  
Tyler Barnhardt ◽  
Ganesh Ambigapathy ◽  
...  
Keyword(s):  
Streptococcus Pneumoniae ◽  
Protective Effect ◽  
Allergic Asthma ◽  
Allergic Inflammation

scholarly journals SERPINB10 contributes to asthma by inhibiting the apoptosis of allergenic Th2 cells

2021 ◽  
Vol 22 (1) ◽  
Author(s):  
Yuqing Mo ◽  
Ling Ye ◽  
Hui Cai ◽  
Guiping Zhu ◽  
Jian Wang ◽  
...  
Keyword(s):  
T Cells ◽  
Allergic Asthma ◽  
Cd4 T Cells ◽  
Quantitative Polymerase Chain Reaction ◽  
Allergic Inflammation ◽  
Specific Ige ◽  
Th2 Cells ◽  
Th1 Cells ◽  
Th2 Response ◽  
Th1 And Th2

Abstract Background Serine peptidase inhibitor, clade B, member 10 (SERPINB10) contributes to allergic inflammation in asthma. However, its role in the T-helper type 2 (Th2) response of allergic asthma is not known. The goal of this study was to unveil the function of SERPINB10 in the Th2 response of allergic asthma and the mechanism by which SERPINB10 affects the viability of Th2 cells. Methods Th2 cytokines and serum levels of house dust mite (HDM)-specific IgE in bronchoalveolar lavage fluid were examined by ELISA in an HDM-induced asthma model. The number and apoptosis of Th1 and Th2 cells in mouse lungs were measured by flow cytometry. Naïve CD4 T cells from patients with asthma were cultured under appropriate polarizing conditions to generate Th1 and Th2 cells. SERPINB10 expression in polarized Th1 and Th2 cells was quantified by real-time reverse transcription-quantitative polymerase chain reaction. SERPINB10 expression was knocked down in human CD4 T cells with lentivirus. Results Knockdown of SERPINB10 expression significantly diminished HDM-induced Th2 cytokine secretion and level of HDM-specific IgE. After HDM exposure, SERPINB10-knockdown mice had diminished numbers of Th2 cells, but similar numbers of Th1 cells, compared with those in negative-control mice. Th2 cells of SERPINB10-knockdown mice were more susceptible to apoptosis than that of control mice. Stimulating T-cell receptors (TCRs) with anti-CD3 antibody caused upregulation of SERPINB10 expression in polarized Th2 cells, but not polarized Th1 cells. Knockdown of SERPINB10 expression resulted in fewer numbers and greater apoptosis of polarized Th2 cells. Conclusion Our results suggest that SERPINB10 may contribute to allergic inflammation and the Th2 response of asthma by inhibiting the apoptosis of Th2 cells.

Protective effect of dietary perilla oil on allergic inflammation in asthmatic mice

2012 ◽  
Vol 114 (9) ◽  
pp. 1007-1015 ◽  
Author(s):  
Hui-Hsiang Chang ◽  
Chin-Shuh Chen ◽  
Jin-Yuarn Lin
Keyword(s):  
Protective Effect ◽  
Allergic Inflammation ◽  
Perilla Oil

scholarly journals Absence of tmRNA has a protective effect against fluoroquinolones in Streptococcus pneumoniae

2020 ◽  
Author(s):  
Liliana Brito ◽  
Joana Wilton ◽  
María José Ferrándiz ◽  
Alicia Gómez Sanz ◽  
Adela G de la Campa ◽  
...  
Keyword(s):  
Streptococcus Pneumoniae ◽  
Protective Effect

scholarly journals Characteristics and Role of Neutrophil Extracellular Traps in Asthma

Inflammation ◽  
2021 ◽  
Author(s):  
Fei Chen ◽  
Min Yu ◽  
Yonghong Zhong ◽  
Lina Wang ◽  
Huaqiong Huang
Keyword(s):  
Systematic Review ◽  
Protective Effect ◽  
Allergic Asthma ◽  
Respiratory Disease ◽  
Bronchial Asthma ◽  
Inflammatory Cells ◽  
Neutrophil Extracellular Traps ◽  
Chronic Respiratory Disease ◽  
Extracellular Traps

Abstract Asthma is a common chronic respiratory disease that affects millions of people worldwide. The incidence of asthma has continued to increase every year. Bronchial asthma involves a variety of cells, including airway inflammatory cells, structural cells, and neutrophils, which have gained more attention because they secrete substances that play an important role in the occurrence and development of asthma. Neutrophil extracellular traps (NETs) are mesh-like structures composed of DNA, histones, and non-histone molecules that can be secreted from neutrophils. NETs can enrich anti-bacterial substances and limit pathogen migration, thus having a protective effect in case of inflammation. However, despite of their anti-inflammatory properties, NETs have been shown to trigger allergic asthma and worsen asthma progression. Here, we provide a systematic review of the roles of NETs in asthma.

scholarly journals Neonatal Streptococcus pneumoniae Pneumonia Induces an Aberrant Airway Smooth Muscle Phenotype and AHR in Mice Model

2019 ◽  
Vol 2019 ◽  
pp. 1-8 ◽  
Author(s):  
Xin Peng ◽  
Yi Wu ◽  
Xiao Kong ◽  
Yunxiu Chen ◽  
Yonglu Tian ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Streptococcus Pneumoniae ◽  
Airway Inflammation ◽  
Allergic Asthma ◽  
Airway Smooth Muscle ◽  
Airway Hyperresponsiveness ◽  
Inflammatory Cells ◽  
Pivotal Role ◽  
Mice Model ◽  
Asthma Model

Our previous study showed that neonatal S. pneumoniae infection aggravated airway inflammation and airway hyperresponsiveness (AHR) in an OVA-induced allergic asthma model. As airway smooth muscle (ASM) plays a pivotal role in AHR development, we aim to investigate the effects of neonatal S. pneumoniae pneumonia on ASM structure and AHR development. Non-lethal neonatal pneumonia was established by intranasally infecting 1-week-old BALB/C mice with the S. pneumoniae strain D39. Five weeks after infection, the lungs were collected to assess the levels of α-SMA and the contractile proteins of ASM. Our results indicate that neonatal S. pneumoniae pneumonia significantly increased adulthood lung α-SMA and SMMHC proteins production and aggravated airway inflammatory cells infiltration and cytokines release. In addition, the neonatal S. pneumoniae pneumonia group had significantly higher Penh values compared to the uninfected controls. These data suggest that neonatal S. pneumoniae pneumonia promoted an aberrant ASM phenotype and AHR development in mice model.

scholarly journals Reduced CCR6+IL-17A+Treg Cells in Blood and CCR6-Dependent Accumulation of IL-17A+Treg Cells in Lungs of Patients With Allergic Asthma

2021 ◽  
Vol 12 ◽  
Author(s):  
Xiaokun Shen ◽  
Huiyun Zhang ◽  
Hua Xie ◽  
Liping Chen ◽  
Shinan Li ◽  
...  
Keyword(s):  
Allergic Asthma ◽  
Treg Cell ◽  
Lung Tissue ◽  
Healthy Subjects ◽  
Allergic Inflammation ◽  
Treg Cells ◽  
Airway Mucosa ◽  
A Cell

Human regulatory T (Treg) cells play a central role in controlling allergic inflammation in the airways. A reduced number of peripheral Treg cells and decreased suppressive function have been previously reported in the pathogenesis of allergic asthma. However, the characteristic role of specific Treg cell subsets and their mechanisms in the pathogenesis of allergic asthma remain unclear. In this study, we examined the proportion of different Treg cell subsets in both healthy subjects and patients with allergic asthma using flow cytometry and single-cell RNA sequencing. The migration function of the cells was compared using cell sorting and Transwell experiments. Furthermore, two allergen-challenged mouse models and a cell transfer experiment were used to examine the role of these Treg subsets. We found that the proportion of CD25+Foxp3+CD127- Treg cells in the peripheral blood of patients with allergic asthma was lower than in those of healthy subjects. Furthermore, the circulating Treg cells expressed lower levels of CCR6 and IL-17 compared with healthy subjects. The chemokine from the airway mucosa, CCL20, was abundantly expressed, and Transwell experiments further proved that this chemokine promoted CCR6+ Treg cell migration in vitro. A mouse model induced by house dust mite (HDM) revealed that the number of CCR6+ Treg cells in the lung tissue increased remarkably. The incidence of allergic asthma may be related to an increase in Treg cells secreting IL-17 in the lung tissue. Recruited CCR6+ Treg cells are likely to differentiate into Th17-like cells under the Th17 environment present in the lungs. IL-17 derived from Th17-like cells could be associated with the pathology of allergic asthma by promoting Th17 responses, thereby favoring HDM-induced asthma exacerbations.

scholarly journals Serotonin 5-HT2receptor activation prevents allergic asthma in a mouse model

2015 ◽  
Vol 308 (2) ◽  
pp. L191-L198 ◽  
Author(s):  
Felix Nau ◽  
Justin Miller ◽  
Jordy Saravia ◽  
Terry Ahlert ◽  
Bangning Yu ◽  
...  
Keyword(s):  
Mouse Model ◽  
Allergic Asthma ◽  
Small Molecule ◽  
Primary Cultures ◽  
Allergic Inflammation ◽  
Inflammatory Processes ◽  
Inhaled Glucocorticoids ◽  
Precise Role ◽  
Airways Inflammation

Asthma is an inflammatory disease of the lung characterized by airways hyper-responsiveness (AHR), inflammation, and mucus hyperproduction. Current mainstream therapies include bronchodilators that relieve bronchoconstriction and inhaled glucocorticoids to reduce inflammation. The small molecule hormone and neurotransmitter serotonin has long been known to be involved in inflammatory processes; however, its precise role in asthma is unknown. We have previously established that activation of serotonin 5-hydroxytryptamine (5-HT)2Areceptors has potent anti-inflammatory activity in primary cultures of vascular tissues and in the whole animal in vasculature and gut tissues. The 5-HT2Areceptor agonist, ( R)-2,5-dimethoxy-4-iodoamphetamine [( R)-DOI] is especially potent. In this work, we have examined the effect of ( R)-DOI in an established mouse model of allergic asthma. In the ovalbumin mouse model of allergic inflammation, we demonstrate that inhalation of ( R)-DOI prevents the development of many key features of allergic asthma, including AHR, mucus hyperproduction, airways inflammation, and pulmonary eosinophil recruitment. Our results highlight a likely role of the 5-HT2receptors in allergic airways disease and suggest that 5-HT2receptor agonists may represent an effective and novel small molecule-based therapy for asthma.

scholarly journals March1 E3 Ubiquitin Ligase Modulates Features of Allergic Asthma in an Ovalbumin-Induced Mouse Model of Lung Inflammation

2018 ◽  
Vol 2018 ◽  
pp. 1-17 ◽  
Author(s):  
Osama A. Kishta ◽  
Antoine Sabourin ◽  
Leora Simon ◽  
Toby McGovern ◽  
Maxime Raymond ◽  
...  
Keyword(s):  
Allergic Asthma ◽  
Mhc Class Ii ◽  
T Cell Activation ◽  
Ubiquitin Ligase ◽  
Cell Activation ◽  
E3 Ubiquitin Ligase ◽  
Allergic Inflammation ◽  
Serum Levels ◽  
Specific Ige ◽  
Cell Surface Expression

Membrane-associated RING-CH-1 (March1) is a member of the March family of E3 ubiquitin ligases. March1 downregulates cell surface expression of MHC II and CD86 by targeting them to lysosomal degradation. Given the key roles of MHC class II and CD86 in T cell activation and to get further insights into the development of allergic inflammation, we asked whether March1 deficiency exacerbates or attenuates features of allergic asthma in mice. Herein, we used an acute model of allergy to compare the asthmatic phenotype of March1-deficient and -sufficient mice immunized with ovalbumin (OVA) and later challenged by intranasal instillation of OVA in the lungs. We found that eosinophilic inflammation in airways and lung tissue was similar between WT and March1−/− allergic mice, whereas neutrophilic inflammation was significant only in March1−/− mice. Airway hyperresponsiveness as well as levels of IFN-γ, IL-13, IL-6, and IL-10 was lower in the lungs of asthmatic March1−/− mice compared to WT, whereas lung levels of TNF-α, IL-4, and IL-5 were not significantly different. Interestingly, in the serum, levels of total and ova-specific IgE were reduced in March1-deficient mice as compared to WT mice. Taken together, our results demonstrate a role of March1 E3 ubiquitin ligase in modulating allergic responses.

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