Modulation of airway hyperresponsiveness by thiols in a murine in vivo model of allergic asthma

2003 ◽  
Vol 52 (3) ◽  
pp. 126-131 ◽  
Author(s):  
J. Kloek ◽  
I. Van Ark ◽  
F. De Clerck ◽  
N. Bloksma ◽  
F. P. Nijkamp ◽  
...  
Keyword(s):  
Allergic Asthma ◽  
Airway Hyperresponsiveness ◽  
In Vivo Model

scholarly journals Calcium-sensing receptor antagonists abrogate airway hyperresponsiveness and inflammation in allergic asthma

2015 ◽  
Vol 7 (284) ◽  
pp. 284ra60-284ra60 ◽  
Author(s):  
Polina L. Yarova ◽  
Alecia L. Stewart ◽  
Venkatachalem Sathish ◽  
Rodney D. Britt ◽  
Michael A. Thompson ◽  
...  
Keyword(s):  
Allergic Asthma ◽  
Airway Hyperresponsiveness ◽  
Eosinophil Cationic Protein ◽  
Adenosine Monophosphate ◽  
Asthma Severity ◽  
Mitogen Activated Protein Kinase ◽  
Calcium Sensing Receptor ◽  
Cationic Protein ◽  
Calcium Sensing

Airway hyperresponsiveness and inflammation are fundamental hallmarks of allergic asthma that are accompanied by increases in certain polycations, such as eosinophil cationic protein. Levels of these cations in body fluids correlate with asthma severity. We show that polycations and elevated extracellular calcium activate the human recombinant and native calcium-sensing receptor (CaSR), leading to intracellular calcium mobilization, cyclic adenosine monophosphate breakdown, and p38 mitogen-activated protein kinase phosphorylation in airway smooth muscle (ASM) cells. These effects can be prevented by CaSR antagonists, termed calcilytics. Moreover, asthmatic patients and allergen-sensitized mice expressed more CaSR in ASMs than did their healthy counterparts. Indeed, polycations induced hyperreactivity in mouse bronchi, and this effect was prevented by calcilytics and absent in mice with CaSR ablation from ASM. Calcilytics also reduced airway hyperresponsiveness and inflammation in allergen-sensitized mice in vivo. These data show that a functional CaSR is up-regulated in asthmatic ASM and targeted by locally produced polycations to induce hyperresponsiveness and inflammation. Thus, calcilytics may represent effective asthma therapeutics.

Anti-inflammatory effect of Rosa laevigata extract on in vitro and in vivo model of allergic asthma via the suppression of IgE and related cytokines

2020 ◽  
Vol 16 (2) ◽  
pp. 119-127 ◽  
Author(s):  
Seung-Hyeon Lee ◽  
Seung-Han Choi ◽  
In-Seung Lee ◽  
Yumi Kim ◽  
Eun-Jin An ◽  
...  
Keyword(s):  
Allergic Asthma ◽  
In Vivo Model ◽  
Anti Inflammatory ◽  
Rosa Laevigata ◽  
Inflammatory Effect

scholarly journals Alcohol reduces airway hyperresponsiveness (AHR) and allergic airway inflammation in mice

2012 ◽  
Vol 302 (3) ◽  
pp. L308-L315 ◽  
Author(s):  
Peter J. Oldenburg ◽  
Jill A. Poole ◽  
Joseph H. Sisson
Keyword(s):  
Mouse Model ◽  
Airway Inflammation ◽  
Allergic Asthma ◽  
Airway Hyperresponsiveness ◽  
Immunoglobulin E ◽  
Allergic Airway Inflammation ◽  
Alcohol Exposure ◽  
Lung Pathology ◽  
Cell Counts

There is very limited knowledge about the effects of alcohol on airway hyperresponsiveness and inflammation in asthma. Historical accounts of alcohol administration to patients with breathing problems suggest that alcohol may have bronchodilating properties. We hypothesized that alcohol exposure will alter airway hyperresponsiveness (AHR) and pulmonary inflammation in a mouse model of allergic asthma. To test this hypothesis, BALB/c mice were fed either 18% alcohol or water and then sensitized and challenged with ovalbumin (OVA). AHR was assessed by means of ventilation or barometric plethysmography and reported as either total lung resistance or enhanced pause, respectively. Airway inflammation was assessed by total and differential cell counts in bronchoalveolar lavage fluid (BALF), cytokine levels in BALF, lung histology, and serum immunoglobulin E (IgE) levels. Alcohol feeding significantly blocked methacholine-induced increases in AHR compared with water-fed controls. Alcohol feeding significantly reduced total cell numbers (64%) as well as the number of eosinophils (84%) recruited to the lungs of these mice. Modest changes in lung pathology were also observed. Alcohol exposure led to a reduction of IgE in the serum of the EtOH OVA mice. These data demonstrate that alcohol exposure blunts AHR and dampens allergic airway inflammation indices in allergic mice and suggest that there may be an important role for alcohol in the modulation of asthma. These data provide an in vivo basis for previous clinical observations in humans substantiating the bronchodilator properties of alcohol and for the first time demonstrates an alcohol-induced reduction of allergic inflammatory cells in a mouse model of allergic asthma.

Establishment of an in vivo model for KCNJ5 dependent hyperaldosteronism

2015 ◽  
Vol 122 (03) ◽  
Author(s):  
U Lichtenauer ◽  
PL Schmid ◽  
A Oßwald ◽  
I Renner-Müller ◽  
M Reincke ◽  
...  
Keyword(s):  
In Vivo Model

An in vivo Model for the Assessment of Acute Fibrinolytic Capacity of the Endothelium

1997 ◽  
Vol 78 (04) ◽  
pp. 1242-1248 ◽  
Author(s):  
David E Newby ◽  
Robert A Wright ◽  
Christopher A Ludlam ◽  
Keith A A Fox ◽  
Nicholas A Boon ◽  
...  
Keyword(s):  
Blood Flow ◽  
Substance P ◽  
Sodium Nitroprusside ◽  
Plasma Concentrations ◽  
In Vivo Model ◽  
Forearm Circulation ◽  
Von Willebrand ◽  
Local Release ◽  
Willebrand Factor

SummaryThe effects on blood flow and plasma fibrinolytic and coagulation parameters of intraarterial substance P, an endothelium dependent vasodilator, and sodium nitroprusside, a control endothelium independent vasodilator, were studied in the human forearm circulation. At subsystemic locally active doses, both substance P (2-8 pmol/min) and sodium nitroprusside (2-8 μg/min) caused dose-dependent vasodilatation (p <0.001 for both) without affecting plasma concentrations of PAI-1, von Willebrand factor antigen or factor VIII:C activity. Substance P caused local increases in t-PA antigen and activity (p <0.001) in the infused arm while sodium nitroprusside did not. At higher doses, substance P increased blood flow and t-PA concentrations in the noninfused arm. We conclude that brief, locally active and subsystemic infusions of intraarterial substance P cause a rapid and substantial local release of t-PA which appear to act via a flow and nitric oxide independent mechanism. This model should provide a useful and selective method of assessing the in vivo capacity of the forearm endothelium to release t-PA acutely.

Closure of Fetoscopic Access Sites with Amniotic Extracellular Matrix Scaffolds in an In Vivo Model

2006 ◽  
Vol 66 (S 01) ◽  
Author(s):  
N Ochsenbein-Kölble ◽  
J Jani ◽  
G Verbist ◽  
L Lewi ◽  
K Marquardt ◽  
...  
Keyword(s):  
Extracellular Matrix ◽  
In Vivo Model ◽  
Extracellular Matrix Scaffolds
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