scholarly journals Semaphorin 3E Inhibits House Dust Mite–Induced Angiogenesis in a Mouse Model of Allergic Asthma

2019 ◽  
Vol 189 (4) ◽  
pp. 762-772 ◽  
Author(s):  
Nazanin Tatari ◽  
Hesam Movassagh ◽  
Lianyu Shan ◽  
Latifa Koussih ◽  
Abdelilah S. Gounni
Author(s):  
Yao-Tung Wang ◽  
Hsu-Chung Liu ◽  
Hui-Chen Chen ◽  
Yen-Ching Lee ◽  
Tung-Chou Tsai ◽  
...  

2021 ◽  
Vol 2 ◽  
Author(s):  
Ananth K. Kammala ◽  
Canchai Yang ◽  
Reynold A. Panettieri ◽  
Rupali Das ◽  
Hariharan Subramanian

G protein-coupled receptor kinase 2 (GRK2) is an adapter protein that modulates G protein-coupled receptor (GPCR) signaling. It also regulates the functions and activity of other intracellular proteins in many cell types. Accordingly, GRK2 is thought to contribute to disease progression by a variety of mechanisms related to its multifunctional roles. Indeed, GRK2 levels are enhanced in patient samples as well as in preclinical models of several diseases. We have previously shown that GRK2 regulates mast cell functions, and thereby contributes to exacerbated inflammation during allergic reactions. In the current study, we observed that GRK2 levels are enhanced in the lungs of human asthma patients and in mice sensitized to house dust mite extract (HDME) allergen. Consistent with these findings, interleukin (IL)-4 and IL-13 levels were reduced in the lungs of GRK2+/− mice in a HMDE mouse model of asthma. Because Th2 cells are the major source of these cytokines during asthma, we determined the role of GRK2 in regulating T cell-specific responses in our HMDE mouse model. We observed a significant reduction of airway hyperresponsiveness (AHR), lung eosinophil and lymphocyte counts, serum IgE, Th2 cytokines (IL-4 and IL-13), goblet cell hyperplasia and mucus production in mice that had reduced GRK2 expression specifically in T cells. Collectively, our studies reveal an important role for GRK2 in regulating T cell response during asthma pathogenesis and further elucidation of the mechanisms through which GRK2 modulates airway inflammation will lead to the development of new therapeutic strategies for asthma.


2021 ◽  
Vol 17 (1) ◽  
Author(s):  
Shereen A. Baioumy ◽  
Aya Elgendy ◽  
Shereen M. Ibrahim ◽  
Sara I. Taha ◽  
Shaimaa H. Fouad

Abstract Background Increased intestinal permeability, either due to the exposure to antigens in asthmatic patients or due to a barrier defect, plays a critical role in susceptibility to environmental allergens. House dust mite allergy occurs more commonly than any other type of allergy among Egyptian asthmatic patients. Aim To assess the relation between serum zonulin level as a marker of increased intestinal permeability and the severity of house dust mite allergic asthma. Methods A case–control study which included 48 patients with house dust mite allergic asthma and 48 healthy control subjects attending the Allergy and Immunology Unit, Microbiology and Immunology Department, Faculty of Medicine, Zagazig University. Results A statistically significant difference was detected between the two studied groups with respect to serum IgE and serum zonulin levels (p ˂ 0.001 and ˂ 0.001, respectively). The mean serum zonulin was equal to 258.3 ± 153.01 ng/ml in the asthmatic group and 80 ± 13 ng/ml in the control group. Serum zonulin level significantly increased with the increase of asthma severity (p ˂ 0.001). The cut off value of serum zonulin was ≥ 198 ng/ml, and the area under the curve was 0.76. It displayed sensitivity equal to 80% and specificity equal to 71.4%. Its negative predictive value was equal to 83.3%. Conclusion Intestinal barrier dysfunction contributes to the pathogenesis of allergic asthma. Serum zonulin level reflects an increase in intestinal permeability. Zonulin acts as prognostic factor of severity in asthma. Correction of the gut barrier defect may have a potential positive prognostic effect in asthma.


2015 ◽  
Vol 114 (2) ◽  
pp. 134-140.e1 ◽  
Author(s):  
Holger Mosbech ◽  
G. Walter Canonica ◽  
Vibeke Backer ◽  
Frederic de Blay ◽  
Ludger Klimek ◽  
...  

Sign in / Sign up

Export Citation Format

Share Document