脂多糖诱导肺部血管周围空间的炎症。
Lipopolysaccharide induced inflammation in the perivascular space in lungs.
机构信息
Dept. of Functional and Applied Anatomy -4120-, Medical School of Hannover, Carl-Neuberg-Str. 1, 30625, Hannover, Germany.
Immunology Research Group, Departments of Veterinary Biomedical Sciences and Veterinary Microbiology, Western College of Veterinary Medicine, University of Saskatchewan, 52 Campus Drive, Saskatoon, SK, S7N 5B4, Canada.
出版信息
J Occup Med Toxicol. 2008 Jul 30;3:17. doi: 10.1186/1745-6673-3-17.
BACKGROUND
Lipopolysaccharide (LPS) contained in tobacco smoke and a variety of environmental and occupational dusts is a toxic agent causing lung inflammation characterized by migration of neutrophils and monocytes into alveoli. Although migration of inflammatory cells into alveoli of LPS-treated rats is well characterized, the dynamics of their accumulation in the perivascular space (PVS) leading to a perivascular inflammation (PVI) of pulmonary arteries is not well described.
METHODS
Therefore, we investigated migration of neutrophils and monocytes into PVS in lungs of male Sprague-Dawley rats treated intratracheally with E. coli LPS and euthanized after 1, 6, 12, 24 and 36 hours. Control rats were treated with endotoxin-free saline. H&E stained slides were made and immunohistochemistry was performed using a monocyte marker and the chemokine Monocyte-Chemoattractant-Protein-1 (MCP-1). Computer-assisted microscopy was performed to count infiltrating cells.
RESULTS
Surprisingly, the periarterial infiltration was not a constant finding in each animal although LPS-induced alveolitis was present. A clear tendency was observed that neutrophils were appearing in the PVS first within 6 hours after LPS application and were decreasing at later time points. In contrast, mononuclear cell infiltration was observed after 24 hours. In addition, MCP-1 expression was present in perivascular capillaries, arteries and the epithelium.
CONCLUSION
PVI might be a certain lung reaction pattern in the defense to infectious attacks.
背景
香烟烟雾和各种环境及职业性粉尘中含有的脂多糖（LPS）是一种毒性物质，可导致肺部炎症，其特征是中性粒细胞和单核细胞迁移到肺泡中。虽然 LPS 处理大鼠的炎症细胞迁移到肺泡中已得到很好的描述，但它们在导致肺小动脉周围炎症（PVI）的血管周围空间（PVS）中的积累动力学尚未得到很好的描述。
方法
因此，我们研究了 LPS 处理的雄性 Sprague-Dawley 大鼠的 PVS 中中性粒细胞和单核细胞的迁移，这些大鼠通过气管内给予大肠杆菌 LPS 并在 1、6、12、24 和 36 小时后安乐死。对照大鼠用不含内毒素的生理盐水处理。制作 H&E 染色切片，并使用单核细胞标志物和趋化因子单核细胞趋化蛋白-1（MCP-1）进行免疫组织化学染色。使用计算机辅助显微镜对浸润细胞进行计数。
结果
令人惊讶的是，尽管存在 LPS 诱导的肺泡炎，但在每个动物中，血管周围浸润并不是一个恒定的发现。观察到一个明显的趋势，即 LPS 应用后 6 小时内首先出现 PVS 中的中性粒细胞，并且在以后的时间点减少。相反，单核细胞浸润在 24 小时后观察到。此外，MCP-1 表达存在于血管周围毛细血管、动脉和上皮中。
结论
PVI 可能是肺部对感染攻击的一种特定反应模式。
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