Abstract
BackgroundNeurokinins (NKs) participate in asthmatic airway inflammation, but the effects of NKs on airway smooth muscle cells (ASMCs) and those of corticosteroids on NKs are unknown.MethodsTo investigate the effect of budesonide on substance P (NK-1) receptor (NK-1R) expression in the lung and ASMCs, 45 Wistar rats were randomly divided into three groups: control, asthmatic, and budesonide treatment. Aerosolized ovalbumin was used to generate the asthmatic rat model, and budesonide was administered after ovalbumin inhalation. On day 21, bronchial responsiveness tests, bronchoalveolar lavage, and cell counting were conducted. NK-1R protein expression in the lung was investigated by immunohistochemistry and image analysis. Primary rat ASMC cultures were established, and purified ASMCs of the fourth passage were collected for mRNA and protein studies via real-time RT-PCR, immunocytochemistry, and image analysis.ResultsNK-1R mRNA and protein expression in the budesonide treatment group rat’s lung and ASMCs were less than that in the asthmatic group but greater than that in the control group.ConclusionsNK-1R is involved in the pathogenesis of asthma and that budesonide may downregulate the expression of NK-1R in the ASMCs and airways of asthmatic rats, which may alleviate neurogenic airway inflammation.
Highlights
Neurokinins (NKs) participate in asthmatic airway inflammation, but the effects of NKs on airway smooth muscle cells (ASMCs) and those of corticosteroids on NKs are unknown
Inhaled corticosteroid treatment is the cornerstone of pharmacotherapy for persistent asthma [5], and airway smooth muscle cells (ASMCs) are important in the pathogenesis of this disease; NK-1R and neurokinin-2 receptors (NK-2R) expression in human and rat ASMC lung tissue has been confirmed by immunohistochemistry [6,7]
The relationship between inhaled corticosteroids and NK-1R expression is unknown, and in our study, we investigated NK-1R expression in asthmatic rat ASMCs to determine the effect of budesonide treatment on neuropeptide receptor expression
Summary
Neurokinins (NKs) participate in asthmatic airway inflammation, but the effects of NKs on airway smooth muscle cells (ASMCs) and those of corticosteroids on NKs are unknown. NKs have potent effects on airway smooth muscle tone, airway secretion, bronchial circulation, and inflammatory and immune cells via the activation of the neurokinin-1 (NK-1R) and neurokinin-2 receptors (NK-2R); as such, they have been proposed to play an important role in human respiratory conditions such as bronchial asthma and chronic obstructive diseases [2]. Inhaled corticosteroid treatment is the cornerstone of pharmacotherapy for persistent asthma [5], and airway smooth muscle cells (ASMCs) are important in the pathogenesis of this disease; NK-1R and NK-2R expression in human and rat ASMC lung tissue has been confirmed by immunohistochemistry [6,7]. The relationship between inhaled corticosteroids and NK-1R expression is unknown, and in our study, we investigated NK-1R expression in asthmatic rat ASMCs to determine the effect of budesonide treatment on neuropeptide receptor expression
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