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单细胞RNA测序揭示了B细胞动态和骨质细胞激活在与塔拉罗美科सिस相关的骨破坏中

Ru-Fei Wei¹, Xin-Ying Chen², Jun-Hong Zhou³

¹School of Public Health of Guangxi Medical University, No. 22, Shuangyong Road, Qingxiu District, Nanning City, Guangxi Zhuang Autonomous Region 530021, China; School of Basic Medical Sciences of Youjiang Medical University for Nationalities, No. 98, Chengxiang Road, Youjiang District, Baise, Guangxi Zhuang Autonomous Region 531400, China.

Cellular signalling

|March 3, 2025

概括

塔拉罗米科斯感染会通过增加骨质细胞活性和B细胞成熟而导致小鼠的骨破坏. 这种骨损失与线粒体功能障碍和氧化应激有关,可能由MAPK信号通路介导.

科学领域:

菌类学菌类学是指菌类学.
免疫学免疫学免疫学
病理学病理学病理学

背景情况:

塔拉罗米科斯是一种由Talaromyces marneffei (TM) 引起的真菌感染,已知会导致系统性疾病.
骨损伤是各种感染的严重并发症,但塔拉罗美科सिस诱导的骨损失背后的机制尚未完全理解.

研究的目的:

为了研究塔拉罗米科斯对骨破坏的影响.
阐明驱动TM诱导的骨病理的细胞和分子机制.

主要方法:

微型CT,组织学染色 (H&E,TRAP,F-actin) 和西部斑点被用于评估骨破坏和骨质细胞活性.
生物力学测试和·弗雷测试评估了骨完整性和疼痛感知.
单细胞RNA测序,流细胞计和qRT-PCR分析了B细胞种群和功能.
通过ELISA,免疫光学和流动细胞计测量了炎症性细胞因子,反应性氧物种 (ROS) 和线粒体膜潜力.
西方涂抹评估了MAPK信号通路的激活.

主要成果:

在小鼠中,TM感染导致显著的骨损伤,骨质细胞活性增加,生物力学特性降低,疼痛增加.
感染后观察到B细胞群 (原始B细胞,ProB细胞,成熟B细胞) 的显著增加.
TM感染增加了炎症性细胞因子和ROS的产生,同时降低了线粒体膜潜力.
激活了MAPK信号通路 (p38,ERK,JNK),促进了骨质细胞分化.

结论:

在小鼠模型中,Talaromyces marneffei感染会触发B细胞成熟,并加剧骨破坏.
线粒体亡和ROS产生,可能通过氧化酸化和MAPK通路激活,与TM诱导的骨质损失有关.

关键词:

B 细胞 B 细胞 B 细胞骨的破坏骨的破坏在 MAPK 信号通路中.这就是ROSOS ROS.塔拉罗米切斯 (Talaromyces marneffei) 是一个有趣的植物.这就是scRNA-seqq.

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