[非特异性预防和治疗铜绿假单胞菌伤口感染的最佳化小鼠模型[作者的翻译]。

A Mayr, B Himmer, G Baljer, J Sailer
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引用次数: 0

摘要

采用“小鼠致病性”铜绿假单胞菌菌株在人工创面上直接感染小鼠的模型,研究了作为抗原非特异性方法激活铜绿假单胞菌创面感染机制的效果。通过生物诱导剂“PIND-AVI”(m - hp438)进行的主动优化显著降低了治疗动物和安慰剂动物之间的死亡率。以肠外预防应用效果最好。在伤口感染前重复注射四次PIND-AVI,将死亡率从80%(安慰剂动物)降低到26.6%。该制剂的临床治疗应用获得了几乎同样好的结果。伤口感染后的小鼠经4次重复治疗,死亡率由86.6%降至36.6%。参数化诱导剂PIND-AVI在所有实验中均未产生副作用。诱导作用在铜绿假单胞菌伤口感染的模式似乎是复杂的。可能发生非特异性调理增加吞噬,巨噬细胞活性增加和淋巴系统同时受到刺激。另一方面,由于诱导剂刺激了铜绿假单胞菌的t细胞和细胞抗原,介质的非特异性作用也可能发挥作用。然而,这两种机制与特异性和非特异性体液因子的合作可能是相互作用的。到什么程度,一个同时合成的问题。内源性干扰素释放的作用尚不清楚。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
[Nonspecific prophylaxis and therapy of Pseudomonas aeruginosa wound-infections with paramunization using a mouse-model (author's transl)].

The effectiveness of paramunization as a antigen nonspecific method to activate mechanisms against wound-infections due to Pseudomonas aeruginosa was studied using a model of direct infection of mice with a "mice-pathogenic" Ps. aeruginosa strain on artificially set wounds. Active paramunization by means of a biological inducer "PIND-AVI" (M-HP 438) significantly reduced the mortality rate between treated and placebo animals. The best results were obtained by parenteral prophylactic application. A four times repeated injection of PIND-AVI before the wound-infection reduced the mortality rate from 80% (placebo animals) to 26.6%. Almost equally good results were obtained by clinically useful therapeutic application of the preparation. A four times repeated treatment of the mice after wound infection lead to a decrease of mortality rates from 86.6% to 36.6%. The paramunization inducer PIND-AVI caused no side effect in any of the experiments. The mode of inducer action in Pseudomonas aeruginosa wound infections appears to be complex. Increased phagocytosis by nonspecific opsonisation, increased macrophage activity and concurrent stimulation of the lymphopoetic system could possible occur. On the other hand the nonspecific action of mediators could also play a role due to the inducer stimulated T-cells and cellular antigens of Pseudomonas aeruginosa. However both mechanisms in cooperation with specific and nonspecific humoral factors are probably interacting together. To what extent a simultaneous synthesis resp. release of endogeneous interferon plays a role is not known.

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