Bronchial Asthma without Airway Hyperresponsiveness

2015 ◽  
pp. 87-88
Author(s):  
D. C. Staa~nescu ◽  
A. Frans
Keyword(s):  
Bronchial Asthma ◽  
Airway Hyperresponsiveness

scholarly journals A Surrogate Marker of Airway Hyperresponsiveness in Patients with Bronchial Asthma

2014 ◽  
Vol 63 (3) ◽  
pp. 487-488
Author(s):  
Yuta Kono ◽  
Seiko Soeda ◽  
Yuki Okada ◽  
Hiroko Hara ◽  
Kosuke Araki ◽  
...  
Keyword(s):  
Bronchial Asthma ◽  
Airway Hyperresponsiveness ◽  
Surrogate Marker

Transient receptor potential melastatin 8 gene polymorphism is associated with cold-induced airway hyperresponsiveness in bronchial asthma

Respirology ◽  
2015 ◽  
Vol 20 (8) ◽  
pp. 1192-1197 ◽  
Author(s):  
Denis E Naumov ◽  
Juliy M Perelman ◽  
Victor P Kolosov ◽  
Tatyana A Potapova ◽  
Vladimir N Maksimov ◽  
...  
Keyword(s):  
Gene Polymorphism ◽  
Bronchial Asthma ◽  
Airway Hyperresponsiveness ◽  
Transient Receptor Potential ◽  
Receptor Potential ◽  
Transient Receptor Potential Melastatin ◽  
Transient Receptor

Involvement of GATA-3-dependent Th2 lymphocyte activation in airway hyperresponsiveness

2006 ◽  
Vol 290 (6) ◽  
pp. L1045-L1051 ◽  
Author(s):  
Naomi Yamashita ◽  
Hiroyuki Tashimo ◽  
Hirofumi Ishida ◽  
Yukiko Matsuo ◽  
Hidekazu Tamauchi ◽  
...  
Keyword(s):  
T Cells ◽  
T Lymphocytes ◽  
Bronchial Asthma ◽  
Airway Hyperresponsiveness ◽  
Receptor Gene ◽  
Whole Body ◽  
Th2 Cytokines ◽  
Lipoxygenase Inhibitor ◽  
Airway Responses

The pathophysiological characteristics of bronchial asthma consist of chronic inflammation of airways, airway hyperresponsiveness, and bronchoconstriction. Studies have shown that T helper type 2 (Th2) cytokines produced by both T cells and mast cells in the airway contribute substantially to the initiation of inflammation in both experimental and human bronchial asthma. GATA-3 is a transcription factor essential to the production of Th2 cytokines by T lymphocytes. To clarify the role of GATA-3-expressing T cells in the pathophysiology of bronchial asthma, we utilized transgenic (Tg) mice carrying the GATA-3 gene and the ovalbumin (OVA)-specific T cell receptor gene (GATA-3-Tg/OVA-Tg). Mice were intranasally administrated OVA without systemic immunization. Airway responses were analyzed with noninvasive and invasive whole body plethysmographs. GATA-3-Tg/OVA-Tg mice exhibited significantly higher IL-13 and IL-4 protein expression in the airway. Although there were no differences in the types of infiltrating cells between GATA-3-Tg/OVA-Tg and GATA-3-non-Tg/OVA-Tg mice and no significant increase in IgE level in either group compared with nontreated mice, the response after ACh inhalation was significantly elevated in GATA-3-Tg/OVA-Tg on the seventh day of intranasal treatment with OVA. This hyperresponsiveness was inhibited by 5-lipoxygenase inhibitor and IL-13 neutralization, suggesting that airway responses were induced through IL-13 and leukotriene pathway. In conclusion, airway hyperresponsiveness, a characteristic of bronchial asthma, is regulated at the level of GATA-3 transcription by T lymphocytes in vivo.

scholarly journals THE CHANGE OF GOBLET CELLS IN RESPONSE TO COLD BRONCHIAL CHALLENGE IN PATIENTS WITH BRONCHIAL ASTHMA WITH COLD AIRWAY HYPERRESPONSIVENESS

2018 ◽  
Vol 1 (68) ◽  
pp. 8-16 ◽  
Author(s):  
Алексей Пирогов ◽  
Aleksey Pirogov ◽  
Анна Приходько ◽  
Anna Prikhodko ◽  
Юлий Перельман ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Bronchial Asthma ◽  
Airway Hyperresponsiveness ◽  
Secretory Activity ◽  
Bronchial Epithelium ◽  
Normal Structure ◽  
Close Correlation ◽  
Air Exposure ◽  
Bronchial Challenge ◽  
Number Of Cells

Destruction of bronchial epithelium in patients with bronchial asthma (BA) is at the bottom of the mechanism of epithelial dysfunction, mucociliary insufficiency and bronchial remodeling. The aim of the work is to assess the character of changes that happen in the structural organization of cell elements and secretory activity of bronchial goblet epithelium in response to cold bronchial challenge in BA patients with cold airway hyperresponsiveness (CAHR). 28 patients with mild BA took part in the research. In the first day of the research the collection of the induced sputum was done, then the next day there was conducted a standard 3-minute test of isocapnic hyperventilation with cold (-20ºC) air (IHCA), after that the collection of sputum was done again. In cytograms of the sputum the percentage, the degree of destruction and cytolysis intensity of cell elements was determined; the contents of glycoproteins in goblet epithelial cells (GS) was studied. The first group included 14 patients with CAHR, the group of comparison (the 2nd group) included 14 patients with BA who did not have airway response to IHCA (ΔFEV1=-19.9±1.6 and -2.8±1.3%, respectively, p=0.00001). After IHCA in cytograms of the sputum of the patients with CAHR there was an increase of the number of neutrophils in relation to the basic one (from 39.9±2.8 till 54.0±2.3%, respectively, p=0.0004), the decrease of the number of macrophages (from 45.3±3.4 till 31.4±2.6%, p=0.005) without the changes of the number of eosinophils (10.0±2.2 and 10.4±1.6%, p=0.14) against intensified cytolysis (2.4±0.16 and 3.1±0.16%, p=0.0007). There was a decrease of the number of GC in relation to the initial one (from 0.22±0.02 till 0.16±0.02%; p=0.037) without significant changes of the number of epithelial cells (1.6±0.54 and 1.5±1.20%; p=0.97). The total index of destruction of GC was 0.45±0.02 and 0.51±0.02 (p=0.045); the index of cytolysis intensiveness of GC was 0.20±0.04 and 0.20±0.02 (p=0.27). A high number of GC that had a normal structure (0 and 1 class of destruction) as well as an increase of the number of cells in relation to initial values of the number of cells of II class against the absence of changes of III and IV classes of destruction were quite noticeable. Under cytochemical reaction the number of alcian blue stained GC actively synthesizing and secreting glycoproteins in response to IHCA increased in relation to the basic value (from 59.8±3.3 till 70.8±4.0%, p=0.0002, respectively). There was found a close correlation between the intensified production of GC glycoproteins in response to bronchial challenge and intensification of bronchial response (∆FEV1) to IHCA (r=-0.37; p=0.029). Thus, in the patients with BA and CAHR a short-term cold air exposure leads to the increase of the number of neutrophils and the decrease of the number of GC under intensive production of glycoproteins in them.

scholarly journals Involvement of PTEN in airway hyperresponsiveness and inflammation in bronchial asthma

2003 ◽  
Vol 111 (7) ◽  
pp. 1083-1092 ◽  
Author(s):  
Yong-Geun Kwak ◽  
Chang H. Song ◽  
Ho K. Yi ◽  
Pyoung H. Hwang ◽  
Jong-Suk Kim ◽  
...  
Keyword(s):  
Bronchial Asthma ◽  
Airway Hyperresponsiveness

scholarly journals Shuang-Huang-Lian Attenuates Airway Hyperresponsiveness and Inflammation in a Shrimp Protein-Induced Murine Asthma Model

2019 ◽  
Vol 2019 ◽  
pp. 1-9
Author(s):  
Yuan Gao ◽  
Qiaoling Fei ◽  
Ruijuan Qi ◽  
Rui Hou ◽  
Yixin Han ◽  
...  
Keyword(s):  
Mast Cell ◽  
Bronchial Asthma ◽  
Airway Hyperresponsiveness ◽  
Cell Activation ◽  
Underlying Mechanism ◽  
Lavage Fluid ◽  
Mast Cell Activation ◽  
Asthma Treatment ◽  
Th2 Immunity ◽  
Mouse Mast Cell

Shuang-Huang-Lian (SHL), an herbal formula of traditional Chinese medicine, is clinically used for bronchial asthma treatment. Our previous study found that SHL prevented basophil activation to suppress Th2 immunity and stabilized mast cells through activating its mitochondrial calcium uniporter. Sporadic clinical reports that SHL was used for the treatment of bronchial asthma can be found. Thus, in this study, we systematically investigated the effects of SHL on asthmatic responses using a shrimp protein (SP)- induced mouse model. SHL significantly inhibited airway inspiratory and expiratory resistance, and histological studies suggested it reduced thickness of airway smooth muscle and infiltration of inflammation cells. It also could alleviate eosinophilic airway inflammation (EAI), including reducing the number of eosinophils and decreasing eotaxin and eosinophil peroxidase levels in the bronchoalveolar lavage fluid (BALF). Further studies indicated that SHL suppressed SP-elevated mouse mast cell protease-1 and IgE levels, prevented Th2 differentiation in mediastinal lymph nodes, and lowered Th2 cytokine (e.g., IL-4, IL-5, and IL-13) production in BALF. In conclusion, SHL attenuates airway hyperresponsiveness and EAI mainly via the inhibition of mast cell activation and Th2 immunity, which may help to elucidate the underlying mechanism of SHL on asthma treatment and support its clinical use.

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