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铜绿假单胞菌外毒素A:其在伤口愈合延迟中的作用:1992年林德伯格奖

Pseudomonas aeruginosa exotoxin A: its role in retardation of wound healing: the 1992 Lindberg Award.

作者信息

Heggers J P, Haydon S, Ko F, Hayward P G, Carp S, Robson M C

机构信息

Department of Plastic Surgery, University of Texas Medical Branch, Shriners Burns Institute, Galvenston 77550.

出版信息

J Burn Care Rehabil. 1992 Sep-Oct;13(5):512-8.

PMID:1452584
Abstract

Bacterial concentrations greater than 10(5) colony-forming units/gm of tissue prevent wound healing. However, it has not been determined whether it is the number of bacteria or a toxin produced by these organisms that impedes the wound healing process. Pseudomonas aeruginosa (PSAR), a burn wound pathogen, produces a dermonecrotic toxin, exotoxin A. Studies have indicated a role for exotoxin A in the pathogenicity of PSAR. We investigated the role of exotoxin A in the retardation of contraction. Acute granulating wounds were created on 90 Sprague-Dawley rats. The animals were equally divided into six groups and were treated topically as follows: group 1, sham: no infection, no treatment; group 2, exotoxin A; group 3, exotoxin A and antiexotoxin; group 4, autoclaved PSAR 10(6); group 5, 10(6) viable PSAR inoculated in the wound; group 6, 10(6) viable PSAR and antiexotoxin. Wound contraction was measured with the use of planimetry twice a week. Serial biopsies were performed on all wounds. Contraction rates revealed significantly (p < 0.05) retarded closure in the animals treated with exotoxin A and in the viable PSAR group when compared with the rates of the noninfected control groups. Animals treated with exotoxin A plus antiexotoxin A and those treated with live PSAR and antiexotoxin showed contraction rates identical to the control groups. These data suggest that exotoxin A in PSAR infections retards wound healing and that neutralization of the toxin restores the normal healing process.

摘要

每克组织中细菌浓度大于10⁵集落形成单位会阻碍伤口愈合。然而,尚未确定是细菌数量还是这些微生物产生的毒素阻碍了伤口愈合过程。铜绿假单胞菌(PSAR)是一种烧伤创面病原体,可产生一种皮肤坏死毒素——外毒素A。研究表明外毒素A在PSAR的致病性中起作用。我们研究了外毒素A在延缓伤口收缩中的作用。在90只Sprague-Dawley大鼠身上制造急性肉芽创面。将动物平均分为六组,并进行如下局部治疗:第1组,假手术组:无感染,不治疗;第2组,外毒素A组;第3组,外毒素A和抗外毒素组;第4组,高压灭菌的PSAR 10⁶;第5组,在伤口接种10⁶活的PSAR;第6组,10⁶活的PSAR和抗外毒素。每周使用平面测量法测量两次伤口收缩情况。对所有伤口进行连续活检。与未感染的对照组相比,外毒素A处理组和活的PSAR组动物的收缩率显示伤口闭合明显延迟(p<0.05)。用外毒素A加抗外毒素A处理的动物以及用活的PSAR和抗外毒素处理的动物的收缩率与对照组相同。这些数据表明,PSAR感染中的外毒素A会延缓伤口愈合,而毒素的中和可恢复正常愈合过程。

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