{"title":"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。","authors":"M Pinto, T Zehavi-Willner","doi":"","DOIUrl":null,"url":null,"abstract":"<p><p>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.</p>","PeriodicalId":22530,"journal":{"name":"The Japanese journal of experimental medicine","volume":"59 5","pages":"189-96"},"PeriodicalIF":0.0000,"publicationDate":"1989-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"Thermal injury-induced non-specific resistance to fatal Pseudomonas aeruginosa burn-infection in mice.\",\"authors\":\"M Pinto, T Zehavi-Willner\",\"doi\":\"\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><p>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.</p>\",\"PeriodicalId\":22530,\"journal\":{\"name\":\"The Japanese journal of experimental medicine\",\"volume\":\"59 5\",\"pages\":\"189-96\"},\"PeriodicalIF\":0.0000,\"publicationDate\":\"1989-10-01\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"The Japanese journal of experimental medicine\",\"FirstCategoryId\":\"1085\",\"ListUrlMain\":\"\",\"RegionNum\":0,\"RegionCategory\":null,\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"\",\"JCRName\":\"\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"The Japanese journal of experimental medicine","FirstCategoryId":"1085","ListUrlMain":"","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
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.