Abstract
BackgroundAsthma is a complex inflammatory disorder involving the activation and invasion of various immune cells. GPR97 is highly expressed in some immunocytes, including mast cells and eosinophils, which play critical roles in asthma development. However, the role of Gpr97 in regulating airway inflammation in asthma has rarely been reported. In this study, we investigated the potential role of Gpr97 in the development of allergic asthma in mice.MethodsRelevant airway asthmatic mouse models were constructed with both wild-type and Gpr97-/- mice sensitized to 250 μg ovalbumin (OVA). The levels of interleukin IL-4, IL-6 and IFN-γ, which are involved in OVA-induced asthma, in the bronchoalveolar lavage fluid (BALF) and the IgE level in the serum were examined by enzyme-linked immunosorbent assay (ELISA). The invasion of mast cells and eosinophils into lung tissues was assessed by immunohistochemical and eosinophil peroxidase activity assays, respectively. Goblet cell hyperplasia and mucus production were morphologically evaluated with periodic acid-Schiff (PAS) staining.ResultsIn our study, no obvious alteration in the inflammatory response or airway remodeling was found in the Gpr97-deficient mice with OVA-induced asthma. Neither the secretion of cytokines, including IL-4, IL-6 and IFN-γ, nor inflammatory cell recruitment was altered in the Gpr97-deficient mice. Moreover, Gpr97 deficiency did not affect airway remodeling or mucus production in the asthma mouse model.ConclusionOur findings imply that Gpr97 might not be required for the development of airway inflammation in OVA-induced allergic asthma in mice.
Highlights
Asthma is one of the most common chronic lung diseases, and it is characterized by reversible airway obstruction, airway hyperresponsiveness, and airway inflammation [1,2,3]
Neither the secretion of cytokines, including IL-4, IL-6 and IFN-γ, nor inflammatory cell recruitment was altered in the Gpr97-deficient mice
Our findings imply that Gpr97 might not be required for the development of airway inflammation in OVA-induced allergic asthma in mice
Summary
Asthma is one of the most common chronic lung diseases, and it is characterized by reversible airway obstruction, airway hyperresponsiveness, and airway inflammation [1,2,3]. Allergic airway inflammation, including the innate and adaptive immune responses, is a striking feature of asthma and is assumed to be the initiating event of airway remodeling [5,6]. Different immune cells, such as eosinophils, macrophages, T helper type 2 (Th2) cells, and mast cells, are involved in the inflammatory response of asthma [5]. Some cytokines are secreted to promote the activation and invasion of mast cells and eosinophils These two types of immune cells can increase inflammatory reactions by releasing cytokines and regulate airway remodeling by promoting mucus hypersecretion and airflow limitation during the asthma process. We investigated the potential role of Gpr in the development of allergic asthma in mice
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