Arai Chikako, Tatefuji Tomoki, Mizote Akiko, Taniguchi Yoshifumi, Kohno Keizo, Inoue Shin-Ichiro, Ohta Tsunetaka, Fukuda Shigeharu
Fujisaki Institute, Hayashibara Biochemical Laboratories, Inc., 675-1 Fujisaki, Okayama 702-8006, Japan.
In Vivo. 2006 Jan-Feb;20(1):77-83.
We have previously shown that when mouse AgK114 (mAgK114, a glycosylphosphatidylinositol anchored membrane-associated protein) is applied to the wound area, the inflammatory responses in the early recovery phase of damaged tissue are enhanced and wound closure is accelerated. This suggests that mAgK114 has an important effect on skin wound repairing.
Whether mAgK114 supresses the development, in NC/Nga mice, of atopic dermatitis (AD)-like skin lesions induced by repeated application of 2,4,6-trinitrochlorobenzene (picryl chloride, PiCl) was examined under specific pathogen-free conditions.
Histopathologically, the application of mAgK114-ointment to the PiCl-treated NC/Nga mice remarkably suppressed severe lymphocytic infiltration into the epidermis, although total skin severity scores, histological changes in hypertrophy, erosion and infiltration of inflammatory cells into the corium and subcutaneous tissues were comparable between the mAgK114-treated group of mice and the control group.
Our results suggest that mAgK114 would be beneficial for the treatment of atopic dermatitis by suppressing severe lymphocytic infiltration into the epidermis.
我们之前已经表明,当将小鼠AgK114(mAgK114,一种糖基磷脂酰肌醇锚定的膜相关蛋白)应用于伤口部位时,受损组织早期恢复阶段的炎症反应会增强,伤口愈合会加速。这表明mAgK114对皮肤伤口修复具有重要作用。
在无特定病原体条件下,检测mAgK114是否能抑制NC/Nga小鼠因反复涂抹2,4,6-三硝基氯苯(苦基氯,PiCl)诱导的特应性皮炎(AD)样皮肤病变的发展。
组织病理学检查显示,将mAgK114软膏应用于经PiCl处理的NC/Nga小鼠时,显著抑制了严重的淋巴细胞浸润至表皮,尽管mAgK114处理组小鼠与对照组之间的总皮肤严重程度评分、肥大的组织学变化、糜烂以及炎症细胞浸润至真皮和皮下组织的情况相当。
我们的结果表明,mAgK114通过抑制严重的淋巴细胞浸润至表皮,可能对特应性皮炎的治疗有益。