Hirakawa K
Department of Orthopedic Surgery, Yokohama City University School of Medicine, Kanagawa, Japan.
Nihon Seikeigeka Gakkai Zasshi. 1994 Apr;68(4):221-33.
Inflammation of the facsimile synovium was induced by injecting 4 mg of heat-killed Escherichia coli (E. coli) O: 14, 1 mg of lipopolysaccharide (LPS), or 100 U of recombinant interleukin-1 beta (IL-1 beta) into a 7-day-old subcutaneous air-pouch in C 57 Black mice. Saline was used for control animals. A total of 150 mice were used. Hyperplasia in the lining cells (lining greater than 5 cells thick) was induced in the inner layer of 18 of 20 air-pouches (in 9 of 10 mice) at 7 days after injection of E. coli or LPS. The results at 7 days after were significantly higher than those at 3 days after injection of E. coli (11/20 mice) or LPS (5/10). The number of lining layers with neutrophil infiltration reached a maximum 3 days after injection of E. coli (3 days: 10/20, 7 days: 2/20, p < 0.01) or LPS (3 days: 7/10, 7 days: 2/10, p < 0.01). There was a greater number of mononuclear cells in the sublining layers 7 days after injection of E. coli (9/20 mice) or LPS (7/10) than at 3 days (2/20, 3/10), (p < 0.01). There was a higher incidence of mononuclear cells around the post-capillary venules (PCV) at 7 days after injection of E. coli (9/20 mice) or LPS (7/10) than at 1 day (0/20, 0/10), (p < 0.01). There were significantly more mast cells around the PCV at 1 day after injection of E. coli (6.0 +/- 2.1) or LPS (5.0 +/- 1.8) than in the saline controls (1.0 +/- 0.4), (p < 0.01). Immunohistochemical stains for IgG showed more positive cells at 7 days after injection of E. coli (4.0 +/- 1.7) or LPS (4.0 +/- 1.4) than in controls (0.5 +/- 0.2), (p < 0.05). Significantly more exudate (0.5 +/- 0.3 mls) was found in the air-pouch at 1 day after injection with IL-1 beta than at 1 day after in the other groups. In conclusion, these results suggest that the air-pouch model may be very useful for investigating possible roles of arthritogenic agents or cytokines on the acute and/or chronic phases of inflammation in connective tissue.
通过向7日龄C57黑鼠的皮下气袋注射4毫克热灭活大肠杆菌（E. coli）O:14、1毫克脂多糖（LPS）或100单位重组白细胞介素-1β（IL-1β）来诱导传真滑膜炎症。生理盐水用于对照动物。总共使用了150只小鼠。在注射大肠杆菌或LPS后7天，20个气袋中的18个（10只小鼠中的9只）内层出现衬里细胞增生（衬里厚度大于5层细胞）。注射大肠杆菌（11/20只小鼠）或LPS（5/10只小鼠）后7天的结果显著高于注射后3天的结果。注射大肠杆菌（3天：10/20，7天：2/20，p<0.01）或LPS（3天：7/10，7天：2/10，p<0.01）后，中性粒细胞浸润的衬里层数在3天达到最大值。注射大肠杆菌（9/20只小鼠）或LPS（7/10只小鼠）后7天，亚衬里层中的单核细胞数量比3天（2/20，3/10）时更多（p<0.01）。注射大肠杆菌（9/20只小鼠）或LPS（7/10只小鼠）后7天，毛细血管后微静脉（PCV）周围单核细胞的发生率高于1天（0/20，0/10）（p<0.01）。注射大肠杆菌（6.0±2.1）或LPS（5.0±1.8）后1天，PCV周围的肥大细胞明显多于生理盐水对照组（1.0±0.4）（p<0.01）。IgG的免疫组织化学染色显示，注射大肠杆菌（4.0±1.7）或LPS（4.0±1.4）后7天的阳性细胞多于对照组（0.5±0.2）（p<0.05）。注射IL-1β后1天，气袋中的渗出液（0.5±0.3毫升）明显多于其他组注射后1天。总之，这些结果表明气袋模型可能对研究致关节炎因子或细胞因子在结缔组织炎症急性和/或慢性期的可能作用非常有用。
