空气细颗粒物通过补体C3a/C3aR轴诱导上皮细胞炎症  

Ambient fine particulate matter triggers inflammatory responses via C3a/C3aR axis in epithelial cells

作　　者：梁爽[1] 闫冰[1] 王成硕[1] 张罗[1,2] LIANG Shuang;YAN Bing;WANG Chengshuo;ZHANG Luo(Department of Otolaryngology Head and Neck Surgery,Key Laboratory ofOtolaryngology Head and Neck Surgery(Capital Medical University),Beijing Institute of Otolaryngology,Engineering ResearchCenter of Ministry of Education,Beijing Key Laboratory of Nasal Diseases,Research Unit of Diagnosis and Treatment of ChronicNasal Diseases,Chinese Academy of Medical Sciences,Beijing Tongren Hospital,CapitalMedical University,Beijing,100730,China;Department of Allergy,Beijing Tongren Hospital,CapitalMedical University,Beijing,100730,China)

机构地区：[1]首都医科大学附属北京同仁医院耳鼻咽喉头颈外科,耳鼻咽喉头颈科学教育部重点实验室(首都医科大学),北京市耳鼻咽喉科研究所,教育部工程中心,鼻病研究北京市重点实验室,中国医学科学院慢性鼻病创新单元,北京100730 [2]首都医科大学附属北京同仁医院变态反应科,北京100730

出　　处：《中国耳鼻咽喉头颈外科》2023年第6期377-381,共5页Chinese Archives of Otolaryngology-Head and Neck Surgery

基　　金：国家重点研发计划(2022YFC2504100);国家自然科学基金(82025010、81630023、82171108、81900917、81870698);东城区优秀人才计划(2022-dchrcpyzz-3)。

摘　　要：目的探讨空气细颗粒物(PM2.5)诱导上皮细胞炎症反应的潜在机制。方法人正常肺支气管上皮细胞Beas-2b细胞暴露于不同剂量PM2.5(0、25、50、100μg/ml)24 h后,利用实时荧光定量聚合酶链式反应(qRT-PCR)和蛋白印迹法(Western blot)检测细胞中胸腺基质淋巴生成素(thymic stromal lymphopoietin,TSLP)、白细胞介素6(IL-6)、IL-8、IL-1β和粒细胞-巨噬细胞集落刺激因子(granulocyte-macrophage colony-stimulating factor,GM-CSF),以及补体C3(complement component 3)、C3a及其受体C3aR表达水平。并利用C3aR拮抗剂处理Beas-2b细胞验证其对PM2.5诱导的炎症水平的抑制作用。结果PM2.5暴露诱导上皮细胞中TSLP、IL-6、IL-8、IL-1β和GMCSF表达显著上调,并诱导细胞中补体C3、C3a和C3aR的基因和蛋白水平显著增加。而C3aR拮抗剂处理可显著抑制PM2.5诱导的Beas-2b细胞中TSLP、IL-6、IL-8和IL-1β的增加。C3aRA也可下调PM2.5诱导的GMCSF表达增加,但差异无统计学意义。结论PM2.5可能通过补体C3a/C3aR轴诱导上皮细胞炎症反应。OBJECTIVE Aimed to explore the mechanism of ambient fine particulate matter(PM2.5)-triggered inflammatory responses in Beas-2b cells.METHODS Beas-2b cells exposed to PM2.5 for 24 h,qRT-PCR,and Western blot assays were used to detect the expression of thymic stromal lymphopoietin(TSLP),interleukin-6(IL-6),IL-8,IL-1βand granulocyte-macrophage colony-stimulating factor(GMCSF),as well as complement component 3(C3)and its receptor(C3aR).Then,the C3aR antagonist(C3aRA)treated with Beas-2b cells verified the suppressed effects on PM2.5-induced inflammatory response.RESULTS The expression of TSLP,IL-6,IL-8,IL-1β,and GM-CSF was significantly increased after exposure to PM2.5 in Beas-2b cells.PM2.5 exposure significantly upregulated the gene and protein levels of C3,C3a,and C3aR.However,the elevation of TSLP,IL-6,IL-8,and IL-1βinduced by PM2.5,could be dramatically suppressed after C3aRA treatment.In addition,C3aRA also downregulated PM2.5-triggered GMCSF increasing,but with no significant difference.CONCLUSION PM2.5 could elicit epithelial inflammation via C3a/C3aR axis.

关 键 词：颗粒物 上皮细胞 支气管 肺 补体C3 炎症 空气细颗粒物 BEAS-2B细胞 

分 类 号：R56[医药卫生—呼吸系统] X513[医药卫生—内科学]