Asanuma Yumiko, Ishimaru Hironobu, Sato Tetsuko, Yamamoto Takenobu, Aoyama Yumi
Department of Dermatology, Kawasaki Medical School, Kurashiki, Okayama, Japan.
Department of Pharmacology, Kawasaki Medical School, Kurashiki, Okayama, Japan.
J Dermatol Sci. 2022 Sep;107(3):151-159. doi: 10.1016/j.jdermsci.2022.09.001. Epub 2022 Sep 5.
Given that ocular glands become infected secondarily to herpes simplex virus 1 (HSV-1) keratitis, resulting in the loss of tear production, sweat glands may also be susceptible to HSV-1 infection, resulting in sweating disturbance, which is observed frequently in atopic dermatitis. However, due to the lack of sweat glands on the hairy skin of mice, the role of sweating in the maintenance of skin hydration has not been elucidated.
To determine the relationship between HSV-1 infection of sweat glands and sweating disturbance-induced dry skin.
By using the impression mold technique, we examined the sweating response together with the detection of HSV-1 DNA in the sweat glands of footpads, the only area with sweat glands in mice, after local cutaneous HSV-1 inoculation of immunocompetent mice.
The sweating response and skin surface hydration were significantly decreased at 7-14 days post-infection. Sweating disturbance and dry skin was markedly enhanced when HSV-1 inoculation was followed by hyperthermic stress. Both resolved spontaneously and became resistant to a second HSV-1 inoculation, associated with increased anti-HSV-IgG antibodies. HSV-1 DNA was detected in sweat glands and dorsal root ganglia. The sweating response remained decreased after subcutaneous injection with pilocarpine, correlating histologically with marked dilatation of sweat gland lumens. These findings indicate that sweating disturbance is unlikely to be the outcome of nerve damage by HSV-1 infection.
Sweating disturbance could be due to HSV-induced dysfunction of sweat glands. We developed a sweating disturbance-induced dry skin mouse model by infection with HSV-1.
鉴于眼部腺体继发于单纯疱疹病毒1型（HSV-1）角膜炎而感染，导致泪液分泌减少，汗腺也可能易受HSV-1感染，从而导致出汗障碍，这在特应性皮炎中经常观察到。然而，由于小鼠有毛皮肤缺乏汗腺，出汗在维持皮肤水合作用中的作用尚未阐明。
确定汗腺的HSV-1感染与出汗障碍引起的皮肤干燥之间的关系。
通过使用印模技术，在对免疫活性小鼠进行局部皮肤HSV-1接种后，我们检查了出汗反应以及小鼠脚垫（小鼠唯一有汗腺的部位）汗腺中HSV-1 DNA的检测情况。
感染后7-14天，出汗反应和皮肤表面水合作用显著降低。在HSV-1接种后施加热应激时，出汗障碍和皮肤干燥明显加剧。两者均自发缓解，并对第二次HSV-1接种产生抗性，同时抗HSV-IgG抗体增加。在汗腺和背根神经节中检测到HSV-1 DNA。皮下注射毛果芸香碱后出汗反应仍然降低，组织学上与汗腺管腔明显扩张相关。这些发现表明出汗障碍不太可能是HSV-1感染导致神经损伤的结果。
出汗障碍可能是由于HSV诱导的汗腺功能障碍。我们通过HSV-1感染建立了一种出汗障碍引起的皮肤干燥小鼠模型。
