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皮肤溃疡的发病机制:从 Mycobacterium ulcerans 和 Leishmania spp. 病原体中得到的启示。

Pathogenesis of skin ulcers: lessons from the Mycobacterium ulcerans and Leishmania spp. pathogens.

机构信息

Unité d'Immunobiologie de l'Infection, Institut Pasteur, 25 Rue du Dr Roux, 75724, Paris Cedex 15, France.

出版信息

Cell Mol Life Sci. 2014 Jul;71(13):2443-50. doi: 10.1007/s00018-014-1561-z. Epub 2014 Jan 21.

Abstract

Skin ulcers are most commonly due to circulatory or metabolic disorders and are a major public health concern. In developed countries, chronic wounds affect more than 1 % of the population and their incidence is expected to follow those observed for diabetes and obesity. In tropical and subtropical countries, an additional issue is the occurrence of ulcers of infectious origins with diverse etiologies. While the severity of cutaneous Leishmaniasis correlates with protective immune responses, Buruli ulcers caused by Mycobacterium ulcerans develop in the absence of major inflammation. Based on these two examples, this review aims to demonstrate how studies on microorganism-provoked wounds can provide insight into the molecular mechanisms controlling skin integrity. We highlight the potential interest of a mouse model of non-inflammatory skin ulceration caused by intradermal injection of mycolactone, an original lipid toxin with ulcerative and immunosuppressive properties produced by M. ulcerans.

摘要

皮肤溃疡通常是由于循环或代谢紊乱引起的,是一个主要的公共卫生问题。在发达国家,慢性伤口影响超过 1%的人口,其发病率预计将与糖尿病和肥胖症的发病率一致。在热带和亚热带国家,另一个问题是出现了具有不同病因的感染性溃疡。虽然皮肤利什曼病的严重程度与保护性免疫反应相关,但由溃疡分枝杆菌引起的伯里溃疡在没有明显炎症的情况下发生。基于这两个例子,本综述旨在展示研究微生物引起的伤口如何深入了解控制皮肤完整性的分子机制。我们强调了通过皮内注射粘菌素引起非炎症性皮肤溃疡的小鼠模型的潜在意义,粘菌素是一种具有溃疡性和免疫抑制特性的原始脂类毒素,由溃疡分枝杆菌产生。

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Treatment of chronic wounds.慢性伤口的治疗。
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