热损伤诱导小鼠对致命铜绿假单胞菌烧伤感染的非特异性抗性。

M Pinto, T Zehavi-Willner
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摘要

通过在烧伤部位的皮肤上立即注射10(3)个活的铜绿假单胞菌,小鼠的非致死性热损伤导致快速死亡。对致死性烧伤合并铜绿假单胞菌感染的抗性在初始热伤后24 h出现,7 d后达到最大;然后持续了至少21天。当在350℃下进行第一次热损伤7秒时,获得了最佳的存活。增加了抗性,但在烧伤前1-4天注射脂多糖(LPS)也可以获得短时间的抗性。绿脓杆菌感染。然而,烧伤感染后立即注射LPS,其致死效应增加。仅铜绿假单胞菌就能诱导热损伤和细菌感染后的后期保护。在相似的热害处理条件下,塞姆利基林病毒侵染均未诱导抗性。相反,病毒感染增加了烧伤小鼠对致命结果的易感性。烧伤后小鼠血清中的免疫抗体和天然抗体均未升高。此外,迟发性超敏反应(通过脚垫重量测定)被抑制,这种抑制至少持续7天。烧伤后7 d,热损伤小鼠胸腺重量和淋巴细胞含量显著降低,脾脏重量增加,每克组织淋巴细胞含量减少。我们认为,烧伤后进入体循环的内毒素可能是早期敏感和晚期保护致死性铜绿假单胞菌烧伤感染的因素之一。
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Thermal injury-induced non-specific resistance to fatal Pseudomonas aeruginosa burn-infection in mice.

Nonlethal thermal injury in mice results in rapid death by immediate injection of 10(3) viable P. aeruginosa in the skin of the burn sites. Resistance to the lethal burn combined with P. aeruginosa infection developed 24 h after initial thermal injury and reached maximal effect 7 days later; it then continued for at least 21 days. The optimal survival was achieved when the first thermal injury was made for 7 seconds at 350 degrees C. Increased resistance, but for a short period could also be obtained by injection of lipopolysaccharide (LPS) 1-4 days prior to the burn-P. aeruginosa infection. However, when the LPS was injected immediately after the burn-infection, the lethal effect was increased. The induction of late protection after thermal injury and bacterial infection was demonstrated with P. aeruginosa organisms only. Under similar schedule of thermal injury resistance was not induced by infection with Semliki forest virus. On the contrary viral infection increased the susceptibility of burned mice to a fatal outcome. Immune or natural antibodies were not elevated in the sera of post burn mice. Furthermore, delayed type hypersensitivity response, as evaluated by a footpad weight assay was inhibited and this inhibition persisted at least for 7 days post burn. The thymus weight and its lymphoid cell content in thermally injured mice decreased significantly 7 days post burn, whereas the weight of the spleen increased and it contained fewer lymphocytes per gram tissue. We suggest that endotoxin entering the systemic circulation post-burn might be one of the factors contributing to the early sensitivity and the late protection against the fatal P. aeruginosa burn-infection.

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