Shi Jue-Ping, Li Xiao-Ning, Zhang Xiao-Yu, Du Bing, Jiang Wen-Zheng, Liu Ming-Yao, Wang Jin-Jin, Wang Zhu-Gang, Ren Hua, Qian Min
Shanghai Key Laboratory of Regulatory Biology, School of Life Sciences, East China Normal University, Shanghai, China; Institute of Biomedical Sciences, School of Life Sciences, East China Normal University, Shanghai, China.
Shanghai Research Center for Model Organisms, Shanghai, China.
PLoS One. 2015 Jul 1;10(7):e0131461. doi: 10.1371/journal.pone.0131461. eCollection 2015.
Asthma 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.
Relevant 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.
In 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.
Our findings imply that Gpr97 might not be required for the development of airway inflammation in OVA-induced allergic asthma in mice.
哮喘是一种复杂的炎症性疾病，涉及多种免疫细胞的激活和浸润。GPR97在包括肥大细胞和嗜酸性粒细胞在内的一些免疫细胞中高表达，这些细胞在哮喘发展中起关键作用。然而，Gpr97在调节哮喘气道炎症中的作用鲜有报道。在本研究中，我们探究了Gpr97在小鼠过敏性哮喘发展中的潜在作用。
用250μg卵清蛋白（OVA）致敏野生型和Gpr97基因敲除小鼠，构建相关气道哮喘小鼠模型。通过酶联免疫吸附测定（ELISA）检测支气管肺泡灌洗液（BALF）中参与OVA诱导哮喘的白细胞介素IL-4、IL-6和IFN-γ水平以及血清中的IgE水平。分别通过免疫组织化学和嗜酸性粒细胞过氧化物酶活性测定评估肥大细胞和嗜酸性粒细胞向肺组织的浸润情况。用高碘酸-希夫（PAS）染色对杯状细胞增生和黏液分泌进行形态学评估。
在我们的研究中，发现Gpr97基因敲除的OVA诱导哮喘小鼠的炎症反应或气道重塑无明显改变。Gpr97基因敲除小鼠的细胞因子分泌（包括IL-4、IL-6和IFN-γ）和炎症细胞募集均未改变。此外，Gpr97基因缺失不影响哮喘小鼠模型的气道重塑或黏液分泌。
我们的研究结果表明，Gpr97可能不是小鼠OVA诱导的过敏性哮喘气道炎症发展所必需的。
