Yang Xue, Liao Daoyong, Huang Ying, Li Chao, Li Yuan, Deng Zhongliang, He Jun
The Affiliated Nanhua Hospital, Department of Clinical Laboratory, Hengyang Medical School, University of South China, Hengyang, People's Republic of China.
Department of Public Health Laboratory Sciences, School of Public Health, Hengyang Medical School, University of South China, Hengyang, Hunan, People's Republic of China.
J Inflamm Res. 2025 Apr 28;18:5727-5739. doi: 10.2147/JIR.S512408. eCollection 2025.
, a clinically significant respiratory pathogen, primarily causes community-acquired pneumonia and contributes to asthma development, with its persistent infection frequently resulting in fibrotic pulmonary changes and structural airway abnormalities. This study investigates the signaling pathways regulating CCL20 expression in THP-1 cells following infection and its impact on cell migration and epithelial-mesenchymal transition (EMT).
THP-1 cells were infected with , and the expression of CCL20 was measured over time and at various doses. In addition, co-culture experiments were performed using -infected THP-1 cells and bronchial epithelial cells to assess EMT and cell migration.
infection significantly upregulated CCL20 production in THP-1 cells via the AKT-ERK1/2-AP1 pathway, a process that was both time- and dose-dependent. Furthermore, co-culturing -infected THP-1 cells with 16HBE cells promoted EMT and increased cell migration, a process that is believed to be associated with CCL20.
This study provides insights into the molecular mechanisms linking CCL20 to cell migration, highlighting potential therapeutic targets for -related lung diseases.
作为一种具有临床意义的呼吸道病原体，主要引起社区获得性肺炎并促进哮喘发展，其持续感染常导致肺纤维化改变和气道结构异常。本研究调查感染后调节THP-1细胞中CCL20表达的信号通路及其对细胞迁移和上皮-间质转化（EMT）的影响。
用感染THP-1细胞，在不同时间和不同剂量下测量CCL20的表达。此外，使用感染的THP-1细胞和支气管上皮细胞进行共培养实验，以评估EMT和细胞迁移。
感染通过AKT-ERK1/2-AP1途径显著上调THP-1细胞中CCL20的产生，这一过程具有时间和剂量依赖性。此外，将感染的THP-1细胞与16HBE细胞共培养可促进EMT并增加细胞迁移，这一过程被认为与CCL20有关。
本研究深入了解了将CCL20与细胞迁移联系起来的分子机制，突出了相关肺部疾病的潜在治疗靶点。
