Matsui Katsuhiko, Tachioka Kanta, Onodera Kei, Ikeda Reiko
Department of Microbial Science and Host Defense, Meiji Pharmaceutical University, Tokyo, Japan.
J Pharm Pharm Sci. 2017;20:38-47. doi: 10.18433/J3GW3D.
Patients with atopic dermatitis (AD) have superficial skin colonization by Staphylococcus aureus and an increased number of T helper type 2 (Th2) cells in their peripheral blood. Our previous study showed that josamycin, a macrolide antibiotic, had excellent bactericidal activity against S. aureus strains isolated from AD patients and simultaneously inhibited Th1 and Th2 cell development mediated by Langerhans cells. The purpose of the present study was to evaluate the effect of topical application of josamycin on AD-like skin lesions in NC/Nga mice.
Josamycin (0.1%) was topically administered to NC/Nga mice with AD-like skin lesions induced by 2, 4, 6-trinitrochlorobenzene (TNCB). The therapeutic effects of josamycin were assessed by measurement of the skin severity scores, histological changes in the lesioned skin, serum levels of total IgE, and expression of interferon (IFN)-γ and interleukin (IL)-4 in lymph nodes and skin lesions.
Topical treatment with josamycin significantly suppressed the increase in the skin severity score in NC/Nga mice. This suppressive effect was equal to that of betamethasone, and was associated with a decrease in the density of cellular infiltration into the dermis, the mast cell count in the dermis and the serum IgE level. Furthermore, topical application of josamycin reduced the expression of IFN-γ and IL-4 in auricular lymph node cells and the skin lesions.
The present results show that topical application of josamycin inhibits the development of AD-like skin lesions in NC/Nga mice. This suggests that topical application of josamycin to AD lesions colonized by S. aureus would be beneficial for control of AD by acting on superficially located S. aureus and by inhibiting the development of Th1 and Th2 cells.This article is open to POST-PUBLICATION REVIEW. Registered readers (see "For Readers") may comment by clicking on ABSTRACT on the issue's contents page.
特应性皮炎（AD）患者的皮肤表层有金黄色葡萄球菌定植，其外周血中2型辅助性T细胞（Th2）数量增加。我们之前的研究表明，大环内酯类抗生素交沙霉素对从AD患者分离出的金黄色葡萄球菌菌株具有优异的杀菌活性，同时抑制朗格汉斯细胞介导的Th1和Th2细胞发育。本研究的目的是评估局部应用交沙霉素对NC/Nga小鼠AD样皮肤损伤的影响。
将交沙霉素（0.1%）局部应用于由2,4,6-三硝基氯苯（TNCB）诱导产生AD样皮肤损伤的NC/Nga小鼠。通过测量皮肤严重程度评分、损伤皮肤的组织学变化、血清总IgE水平以及淋巴结和皮肤损伤中干扰素（IFN）-γ和白细胞介素（IL）-4的表达来评估交沙霉素的治疗效果。
局部应用交沙霉素可显著抑制NC/Nga小鼠皮肤严重程度评分的增加。这种抑制作用与倍他米松相当，且与真皮层细胞浸润密度、真皮层肥大细胞计数及血清IgE水平的降低有关。此外，局部应用交沙霉素可降低耳淋巴结细胞和皮肤损伤中IFN-γ和IL-4的表达。
目前的结果表明，局部应用交沙霉素可抑制NC/Nga小鼠AD样皮肤损伤的发展。这表明，将交沙霉素局部应用于被金黄色葡萄球菌定植的AD损伤部位，通过作用于表面的金黄色葡萄球菌并抑制Th1和Th2细胞的发育，对控制AD可能有益。本文接受出版后审查。注册读者（见“致读者”）可通过点击本期目录页上的摘要进行评论。
