Mayr A, Himmer B, Baljer G, Sailer J
Zentralbl Bakteriol Orig A. 1979 Sep;244(4):506-14.
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.
使用“小鼠致病性”铜绿假单胞菌菌株对小鼠人工设定伤口进行直接感染的模型,研究了免疫佐剂化作为一种抗原非特异性方法激活针对铜绿假单胞菌伤口感染机制的有效性。通过生物诱导剂“PIND-AVI”(M-HP 438)进行的主动免疫佐剂化显著降低了治疗组和安慰剂组动物之间的死亡率。通过肠胃外预防性应用获得了最佳结果。在伤口感染前四次重复注射PIND-AVI将死亡率从80%(安慰剂组动物)降低到26.6%。通过该制剂临床上有用的治疗性应用也获得了几乎同样好的结果。伤口感染后对小鼠进行四次重复治疗导致死亡率从86.6%降至36.6%。免疫佐剂化诱导剂PIND-AVI在任何实验中均未引起副作用。铜绿假单胞菌伤口感染中诱导剂的作用模式似乎很复杂。可能会通过非特异性调理作用增加吞噬作用、增加巨噬细胞活性并同时刺激淋巴细胞生成系统。另一方面,由于诱导剂刺激的T细胞和铜绿假单胞菌的细胞抗原,介质的非特异性作用也可能起作用。然而,这两种机制与特异性和非特异性体液因子协同作用可能共同发挥作用。内源性干扰素的同时合成和释放起到多大作用尚不清楚。