Gpr97 Is Dispensable for Inflammation in OVA-Induced Asthmatic Mice.
Gpr97 Is Dispensable for Inflammation in OVA-Induced Asthmatic Mice.
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Gpr97 对于 OVA 诱发的哮喘小鼠的炎症是可有可无的
DOI：
10.1371/journal.pone.0131461
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发表时间：
2015
期刊：
影响因子：
3.7
通讯作者：
Qian M
中科院分区：
文献类型：
--
作者：
Shi JP;Li XN;Zhang XY;Du B;Jiang WZ;Liu MY;Wang JJ;Wang ZG;Ren H;Qian M
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侵袭。GPR97在一些免疫细胞中高度表达，包括肥大细胞和嗜酸性粒细胞，它们在哮喘的发展中起关键作用。然而，Gpr97在哮喘气道炎症调节中的作用鲜有报道。在本研究中，我们研究了Gpr97在小鼠变应性哮喘发生中的潜在作用。方法采用250 μg卵清蛋白致敏的野生型和Gpr97-/-型小鼠建立相应的气道哮喘小鼠模型。采用酶联免疫吸附试验（ELISA）检测哮喘大鼠支气管肺泡灌洗液（BALF）中与ova诱发哮喘相关的白细胞介素IL-4、IL-6、IFN-γ水平及血清IgE水平。通过免疫组化和嗜酸性粒细胞过氧化物酶活性测定分别评估肥大细胞和嗜酸性粒细胞对肺组织的侵袭。用周期性酸-希夫（PAS）染色观察杯状细胞增生和粘液的产生。结果在我们的研究中，gpr97缺陷小鼠的炎症反应和气道重塑未见明显改变。在gpr97缺陷小鼠中，细胞因子（包括IL-4、IL-6和IFN-γ）的分泌和炎症细胞募集均未发生改变。此外，Gpr97缺乏不影响哮喘小鼠模型的气道重塑或粘液产生。结论在ova诱导的小鼠过敏性哮喘中，Gpr97可能不需要参与气道炎症的发生。
Background 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. Methods 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. Results 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. Conclusion Our findings imply that Gpr97 might not be required for the development of airway inflammation in OVA-induced allergic asthma in mice.
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