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Ccl12协调免疫-神经交叉声调,以促进烧伤创伤后脂肪交感重塑
Chuwei Zhang1, Yanshen Chen2, Jingya Guo2
1College of Pharmacy, China Pharmaceutical University, Nanjing, China; Department of Burn and Plastic Surgery, Department of Wound Repair Surgery, Affiliated Hospital of Nantong University, Nantong, China.
Cell reports
|January 29, 2026
概括
烧伤伤害激活了白色脂肪组织 (WAT) 中的局部免疫神经轴,促进了交感重塑和热能重编程. 这一途径涉及巨细胞和T细胞,影响烧伤后WAT色.
科学领域:
- 免疫学 免疫学 免疫学
- 神经科学是一个神经科学.
- 代谢过程中的代谢.
- 脂肪组织生物学 脂肪组织生物学
背景情况:
- 烧伤伤害导致持续的白色脂肪组织 (WAT) 重塑和超高代谢.
- 系统性甲醇胺是主要的驱动因素,但WAT中的局部机制尚不清楚.
研究的目的:
- 确定驱动燃烧损伤后WAT的同情重塑和热能重编程的局部机制.
- 阐明脂肪内免疫神经轴在这个过程中的作用.
主要方法:
- 鼠伤模型研究烧伤伤害对WAT的影响.
- 化学和遗传脱皮,以评估同情神经系统的参与.
- 巨细胞和T细胞信号通路分析 (Ccl12,CCR2,神经生长因子).
- 对人类烧伤患者的WAT样本进行分析.
主要成果:
- 烧伤诱导局部交感激活,上腺素释放和WAT棕色化在小鼠中,通过消皮消除.
- 巨细胞衍生的Ccl12招募了CCR2+ T细胞,这些细胞分泌神经生长因子,促进了交感神经细胞的增长.
- 破坏这种途径 (Ccl12中和或T细胞缺陷) 损害了WAT棕色化.
- 人体烧伤WAT显示同情性内置增加,解蛋白-1表达和CCR2+T细胞.
结论:
- 脂肪内免疫神经轴在烧伤后调节脂肪组织功能.
- 这条通路对于同情性重塑和WAT棕色化至关重要.
- 在这个轴内,存在调节燃烧诱导的高代谢的潜在治疗点.
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