Pseudomonas aeruginosa exotoxin A: Its role in retardation of wound healing: The 1992 Lindberg award

Pseudomonas aeruginosa exotoxin A: Its role in retardation of wound healing: The 1992 Lindberg award
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DOI:
10.1097/00004630-199209000-00003
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发表时间:
1992-01-01
期刊:
Journal of Burn Care and Rehabilitation
影响因子:
--
通讯作者:
Robson, Martin C.
Robson, Martin C.
中科院分区:
其他
文献类型:
--
作者:
Heggers, John P.;Haydon, Scott;Robson, Martin C.

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细菌浓度大于10-5菌落形成单位/克组织会阻止伤口愈合。然而,还没有确定是否是细菌的数量或这些生物体产生的毒素阻碍了伤口愈合过程。铜绿假单胞菌(PSAR)是一种烧伤创面致病菌,能产生皮肤坏死毒素--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在收缩延迟中的作用。在90只Sprague-Dawley大鼠上制造急性肉芽化伤口。将动物等分为6组,并按如下方式进行局部处理:第1组,假手术:无感染,无处理;第2组,外毒素A;第3组,外毒素A和抗外毒素;第4组,高压灭菌的PSAR 10-6;第5组,在伤口中接种10-6活PSAR;第6组,10-6活PSAR和抗外毒素。每周两次使用面积测量法测量伤口收缩。对所有伤口进行连续活检。与未感染的对照组相比,用外毒素A处理的动物和活的PSAR组的收缩率显示显著(p lt 0.05)延迟闭合。用外毒素A加抗外毒素A处理的动物和用活PSAR和抗外毒素处理的动物显示与对照组相同的收缩率。这些数据表明PSAR感染中的外毒素A延缓伤口愈合,并且毒素的中和恢复正常愈合过程。
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 lt 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.