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细胞外乙化希斯 3.3 诱导炎症和肺组织损伤

Mario C Rico¹, Oscar Perez-Leal¹, Mary F Barbe²

¹Pharmaceutical Sciences Department, Temple University School of Pharmacy, Philadelphia, PA 19140, USA.

|September 28, 2023

概括

细胞外乙化组合素H3.3 (AcH3.3) 在小鼠中显著恶化肺组织损伤和炎症,这表明它在慢性阻塞性肺病 (COPD) 进展中发挥了作用.

科学领域:

肺部医学肺部医学
细胞生物学细胞生物学
免疫学免疫学免疫学

背景情况:

细胞外组织蛋白,损伤相关的分子模式 (DAMPs),从死亡的细胞中释放出来,导致毒性.
慢性阻塞性肺病 (COPD) 肺部表现出丰富的细胞外素H3.3,通常是过化 (AcH3.3).
在COPD引起的肺损伤中,AcH3.3的特定作用尚未完全理解.

研究的目的:

为了研究细胞外乙化组织素H3.3 (AcH3.3) 对肺组织损伤和炎症的影响.
为了确定AcH3.3是否会加剧肺损伤,与非乙化组合素H3.3.3相比.

主要方法:

在小鼠中通过内灌注给予复合组合基因组 (rH2A,rH3.3,rAcH3.3) 或载体.
评估肺组织损伤,组织学变化,亡 (caspase 3和9) 和全身炎症标志物 (TNF-α,IL-6,MCP-3,CXCL-1) 在灌注后48小时.
微型CT分析和对焦成像用于结构变化和免疫细胞透 (淋巴细胞,单细胞/巨细胞).

主要成果:

肺内灌注rAcH3.3导致比rH3.3或车载更严重的肺组织损伤.
组织学分析显示,在接受rAcH3.3治疗的小鼠中,膜壁破裂,上皮损伤和免疫细胞透.
rAcH3.3增加了亡,触发了全身炎症标志物,并导致白细胞和淋巴细胞,确认了淋巴细胞和单细胞/巨细胞的透.

结论:

细胞外AcH3.3诱导肺部显著的细胞毒性和急性炎症反应.
在促进肺组织损伤和炎症方面,AcH3.3起着至关重要的作用.
这些发现表明,AcH3.3是COPD肺损伤进展的潜在驱动因素.

关键词:

慢性慢性肺炎是一种慢性慢性肺炎,COPD是一种慢性肺炎.H3.3 其他类型在HDAC的基础上,HDAC是气泡膜损伤气泡膜损伤细胞因子细胞因子细胞毒性细胞毒性基因组基因组基因组过度乙化过度乙化这是一种炎症炎症炎症炎症.

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