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Inhaled corticosteroids inhibit substance P receptor expression in asthmatic rat airway smooth muscle cells

BACKGROUND: 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. METHODS: To investigate the effect of budesonide on substance P (NK-1) receptor (NK-1R) expression in the lung and...

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Detalles Bibliográficos
Autores principales: Li, Miao, Shang, Yun-xiao
Formato: Online Artículo Texto
Lenguaje:English
Publicado: BioMed Central 2012
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3579708/
https://www.ncbi.nlm.nih.gov/pubmed/23244548
http://dx.doi.org/10.1186/1471-2466-12-79
Descripción
Sumario:BACKGROUND: 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. METHODS: To 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. RESULTS: NK-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. CONCLUSIONS: NK-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.