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断发毛癣菌诱导的角化性脓癣,防御素表达降低,而白细胞介素-17A 产生却增加。

Trichophyton tonsurans-induced kerion celsi with decreased defensin expression and paradoxically increased interleukin-17A production.

机构信息

Division of Dermatology, Fujinomiya City General Hospital, Fujinomiya, Japan.

Division of Dermatology, Shizuoka Municipal Hospital, Shizuoka, Japan.

出版信息

J Dermatol. 2019 Sep;46(9):794-797. doi: 10.1111/1346-8138.15008. Epub 2019 Jul 11.

Abstract

We report a case of kerion celsi due to Trichophyton tonsurans. An 18-year-old male student judo practitioner had alopecic patches, black dots and subcutaneous abscesses on the right temporal region. The damaged hair represented endothrix infection with T. tonsurans, as assessed by mycological examinations. He was treated with oral itraconazole without any therapeutic effect, followed by terbinafine with good effect. A skin biopsy showed neutrophil, lymphocyte and histiocyte infiltration into the dermis and subcutaneous tissue with abscesses around a number of dilated hair follicles. Immunostaining showed that the expression level of human β-defensin 2 (HBD-2) was decreased in the epidermis of the alopecic and adjacent skin. Because interleukin (IL)-17A generally induces HBD-2 production by epidermal keratinocytes, we also immunohistochemically investigated IL-17A expression. Unexpectedly, many IL-17A-bearing cells were found around destructed hair follicles, indicating that IL-17A expression was not attenuated, but rather increased in the skin lesion. Our case suggests that IL-17A-upregulated antimicrobial peptide expression is disordered in kerion celsi, and severe inflammation with IL-17A may cause tissue damage and resultant scar.

摘要

我们报告了一例由须癣毛癣菌引起的脓癣。一名 18 岁男性柔道运动员右颞部有脱发斑、黑点和皮下脓肿。通过真菌学检查,受损毛发表现为内生型感染,为须癣毛癣菌。他曾接受伊曲康唑口服治疗,但无疗效,后改用特比萘芬治疗,效果良好。皮肤活检显示真皮和皮下组织中有中性粒细胞、淋巴细胞和组织细胞浸润,许多扩张的毛囊周围有脓肿。免疫组化染色显示,脱发区和相邻皮肤表皮中人类 β 防御素 2(HBD-2)的表达水平降低。由于白细胞介素(IL)-17A 通常可诱导表皮角质形成细胞产生 HBD-2,我们还进行了 IL-17A 的免疫组化研究。出乎意料的是,在破坏的毛囊周围发现了许多携带 IL-17A 的细胞,表明皮肤病变中 IL-17A 的表达没有减弱,反而增加了。我们的病例提示脓癣中 IL-17A 上调的抗菌肽表达紊乱,IL-17A 引起的严重炎症可能导致组织损伤和瘢痕形成。

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