Role of GM-CSF in a mouse model of experimental autoimmune prostatitis
Role of GM-CSF in a mouse model of experimental autoimmune prostatitis
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GM-CSF 在实验性自身免疫性前列腺炎小鼠模型中的作用
DOI：
10.1152/ajprenal.00013.2018
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发表时间：
2019
期刊：
影响因子：
--
通讯作者：
Shi Benkang
中科院分区：
文献类型：
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作者：
Liu Yaxiao;Li Yan;Liu Qinggang;Wu Zonglong;Cui Jianfeng;Zhu Kejia;Zhao Hongda;Zhou Changkuo;Shi Benkang
慢性前列腺炎/慢性骨盆疼痛综合征（CP/CPPS）的病因尚不清楚。粒细胞巨噬细胞集落刺激因子（GM-CSF）在自身免疫性疾病和炎症性疾病的发生发展中起重要作用。在这里，我们研究了GM-CSF在CP/CPPS患者和实验性自身免疫性前列腺炎（EAP）小鼠模型中的表达和功能。在CP/CPPS患者的前列腺分泌物样品和EAP小鼠模型的前列腺组织中检测GM-CSF mRNA水平。用PCR和免疫组织化学方法检测小鼠前列腺和背根神经节中GM-CSF受体的表达。使用GM-CSF敲除小鼠进行行为测试和炎症评分以评估GM-CSF在EAP的疾病发展和症状严重性中的作用。在诱导EAP后，在前列腺中测量推定的伤害性和炎症性标记物的mRNA水平。与健康志愿者相比，在CP/CPPS患者的前列腺液中观察到GM-CSF mRNA水平升高。在EAP小鼠模型的前列腺组织中GM-CSF mRNA也显著增加。在小鼠前列腺和背根神经节中证实了GM-CSF受体的表达。GM-CSF敲除小鼠在EAP诱导后表现出更少的浸润白细胞和疼痛症状。GM-CSF的缺失显著降低了EAP诱导的趋化因子（C-C基序）配体2、趋化因子（C-C基序）配体3和神经生长因子mRNA表达的增加。结果表明GM-CSF在EAP的发病机制中发挥着功能性作用。在CP/CPPS中，GM-CSF可能作为炎症和疼痛传导的信号介质。
The etiology of chronic prostatitis/chronic pelvic pain syndrome (CP/CPPS) is still unknown. Granulocyte macrophage colony-stimulating factor (GM-CSF) has been shown to play an important role in the development of autoimmune and inflammatory diseases. Here, we investigated the expression and function of GM-CSF in patients with CP/CPPS and in a mouse model of experimental autoimmune prostatitis (EAP). GM-CSF mRNA levels were detected in expressed prostatic secretions samples from patients with CP/CPPS and in prostate tissue from a mouse model of EAP. The expression of GM-CSF receptor in mouse prostate and dorsal root ganglia were determined using PCR and immunohistochemistry. Behavioral testing and inflammation scoring were performed to evaluate the role of GM-CSF in disease development and symptom severity of EAP using GM-CSF knockout mice. mRNA levels of putative nociceptive and inflammatory markers were measured in the prostate after the induction of EAP. Elevated GM-CSF mRNA levels were observed in expressed prostatic secretions samples from patients with CP/CPPS compared with healthy volunteers. GM-CSF mRNA was also significantly increased in prostate tissue of the EAP mice model. The expression of GM-CSF receptors was confirmed in mouse prostate and dorsal root ganglia. GM-CSF knockout mice showed fewer Infiltrating leukocytes and pain symptoms after the induction of EAP. Deletion of GM-CSF significantly diminished EAP-induced increases of chemokine (C-C motif) ligand 2, chemokine (C-C motif) ligand 3, and nerve growth factor mRNA expression. The results indicated that GM-CSF plays a functional role in the pathogenesis of EAP. GM-CSF may function as a signaling mediator for both inflammation and pain transduction in CP/CPPS.