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1
Steroids control paradoxical worsening of Mycobacterium ulcerans infection following initiation of antibiotic therapy.类固醇可控制抗生素治疗开始后溃疡分枝杆菌感染的反常恶化。
Med J Aust. 2013 May 6;198(8):443-4. doi: 10.5694/mja12.11559.
2
Mycolactone activation of Wiskott-Aldrich syndrome proteins underpins Buruli ulcer formation.分枝杆菌酸激活威特综合征蛋白是导致布鲁里溃疡形成的原因。
J Clin Invest. 2013 Apr;123(4):1501-12. doi: 10.1172/JCI66576. Epub 2013 Mar 15.
3
Neural Wiskott-Aldrich syndrome protein (N-WASP)-mediated p120-catenin interaction with Arp2-Actin complex stabilizes endothelial adherens junctions.神经 Wiskott-Aldrich 综合征蛋白 (N-WASP) 介导的 p120 连环蛋白与 Arp2-肌动蛋白复合物的相互作用稳定了内皮细胞黏附连接。
J Biol Chem. 2013 Feb 8;288(6):4241-50. doi: 10.1074/jbc.M112.440396. Epub 2012 Dec 4.
4
Treatment of chronic wounds.慢性伤口的治疗。
Vasa. 2012 Nov;41(6):396-409. doi: 10.1024/0301-1526/a000230.
5
Corticosteroid use for paradoxical reactions during antibiotic treatment for Mycobacterium ulcerans.在溃疡分枝杆菌抗生素治疗期间使用皮质类固醇治疗反常反应。
PLoS Negl Trop Dis. 2012;6(9):e1767. doi: 10.1371/journal.pntd.0001767. Epub 2012 Sep 27.
6
Diagnosis and treatment of Basal cell and squamous cell carcinoma.基底细胞癌和鳞状细胞癌的诊断与治疗。
Am Fam Physician. 2012 Jul 15;86(2):161-8.
7
FasL and TRAIL signaling in the skin during cutaneous leishmaniasis - implications for tissue immunopathology and infectious control.皮肤利什曼病皮肤中的 FasL 和 TRAIL 信号传导——对组织免疫病理学和感染控制的影响。
Front Immunol. 2012 Jun 19;3:163. doi: 10.3389/fimmu.2012.00163. eCollection 2012.
8
Cutaneous leishmaniasis mimicking inflammatory and neoplastic processes: a clinical, histopathological and molecular study of 57 cases.模仿炎症和肿瘤性病变的皮肤利什曼病:57例临床、组织病理学及分子研究
J Cutan Pathol. 2012 Feb;39(2):251-62. doi: 10.1111/j.1600-0560.2011.01844.x. Epub 2011 Dec 15.
9
Paradoxical responses after start of antimicrobial treatment in Mycobacterium ulcerans infection.抗菌治疗开始后分枝杆菌溃疡感染的矛盾反应。
Clin Infect Dis. 2012 Feb 15;54(4):519-26. doi: 10.1093/cid/cir856. Epub 2011 Dec 7.
10
Chemotherapy-associated changes of histopathological features of Mycobacterium ulcerans lesions in a Buruli ulcer mouse model.在布鲁里溃疡小鼠模型中分枝杆菌溃疡病变的组织病理学特征的化疗相关变化。
Antimicrob Agents Chemother. 2012 Feb;56(2):687-96. doi: 10.1128/AAC.05543-11. Epub 2011 Dec 5.

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.

DOI:10.1007/s00018-014-1561-z
PMID:24445815
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11113781/
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。