Mölne L, Tarkowski A
Departments of Dermatology and Rheumatology, Sahlgrenska University Hospital, Göteborg, Sweden.
J Invest Dermatol. 2000 Jun;114(6):1120-5. doi: 10.1046/j.1523-1747.2000.00973.x.
Skin infections caused by Staphylococcus aureus, such as erysipelas, are commonly occurring, painful, and costly for society. Despite the high prevalence of this condition, little is known about the host immune responsiveness and bacterial virulence factors during S. aureus dermatitis. We present here a mouse model of infectious dermatitis in which S. aureus is inoculated by an intracutaneous injection to the shaved back of NMRI mice. Visible skin inflammation, characterized by redness and swelling, was noted 48 h after inoculation of staphylococci in mice that received 2 x 108 colony-forming units of S. aureus. Microscopic evaluation revealed a dermal and subcutaneous infiltrate rich in macrophages and neutrophilic granulocytes already within 6 h after inoculation. A sparse influx of T lymphocytes was noted somewhat later. Bacterial cultures from skin revealed high numbers of staphylococci early after inoculation, with a successive decline during 2 wk follow-up. Total white blood cell count as well as the number of polymorphonuclear leukocytes peaked 2 d after bacterial inoculation. Also, serum interleukin-6 levels peaked within 2 d, with a 10-fold increase compared to non-infected control mice, indicating a systemic reaction to skin infection. The role of toxic shock syndrome toxin 1 in the pathogenesis of the dermatitis was assessed using isogenic S. aureus strains. Even though the gross inflammatory skin reaction was similar for mice infected with either of the strains, it was apparent that bacteria secreting toxic shock syndrome toxin 1 preferentially triggered influx of T lymphocytes to the skin. In addition, mice inoculated with staphylococci producing toxic shock syndrome toxin 1 showed a weight decrease during the experiment whereas mice inoculated with the isogenic strain showed a weight increase. This model of staphylococcal dermatitis will enable future in-depth studies regarding the host-bacterium relationship.
由金黄色葡萄球菌引起的皮肤感染，如丹毒，在社会上普遍存在、令人痛苦且代价高昂。尽管这种疾病的患病率很高，但对于金黄色葡萄球菌性皮炎期间宿主的免疫反应性和细菌毒力因子知之甚少。我们在此展示一种感染性皮炎的小鼠模型，其中通过皮内注射将金黄色葡萄球菌接种到NMRI小鼠剃毛的背部。在接种2×10⁸个金黄色葡萄球菌菌落形成单位的小鼠中，接种葡萄球菌48小时后，可见以发红和肿胀为特征的皮肤炎症。显微镜评估显示，接种后6小时内真皮和皮下就有富含巨噬细胞和嗜中性粒细胞的浸润。稍晚些时候注意到有少量T淋巴细胞流入。皮肤细菌培养显示接种后早期葡萄球菌数量很多，在2周的随访期间逐渐减少。细菌接种后2天，白细胞总数以及多形核白细胞数量达到峰值。此外，血清白细胞介素-6水平在2天内达到峰值，与未感染的对照小鼠相比增加了10倍，表明对皮肤感染有全身反应。使用同基因金黄色葡萄球菌菌株评估了毒性休克综合征毒素1在皮炎发病机制中的作用。尽管感染任何一种菌株的小鼠的总体炎症皮肤反应相似，但显然分泌毒性休克综合征毒素1的细菌优先触发T淋巴细胞流入皮肤。此外，接种产生毒性休克综合征毒素1的葡萄球菌的小鼠在实验期间体重下降，而接种同基因菌株的小鼠体重增加。这种葡萄球菌性皮炎模型将有助于未来对宿主与细菌关系进行深入研究。
