Lipopolysaccharide-induced non-specific resistance to systemic Escherichia coli infection in mice.
Lipopolysaccharide-induced non-specific resistance to systemic Escherichia coli infection in mice.
复制标题
脂多糖诱导小鼠对全身性大肠杆菌感染的非特异性抵抗。
DOI：
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发表时间：
1988
影响因子：
3
通讯作者：
P. Mäkelä
中科院分区：
文献类型：
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作者：
J. Vuopio‐Varkila;M. Nurminen;L. Pyhälä;P. Mäkelä
A high degree of non-specific resistance to a lethal systemic Escherichia coli infection was induced in mice by pretreatment with a small dose (less than 5 micrograms/mouse) of the homologous lipopolysaccharide (LPS) or with heterologous rough-type LPS from E. coli K-12. The route of LPS administration, intraperitoneally or subcutaneously, did not influence the development of resistance, suggesting that a systemic cell activation was responsible for the effect. The enhanced elimination of bacteria was similar to that in mice recovering from a sublethal E. coli infection. In the LPS-treated mice, elimination of the challenge bacteria from the peritoneal cavity and the blood started 3-4 h after challenge whereas, in controls, the bacterial numbers continued to increase until the mice died. The detoxified LPS derivative, monophosphoryl lipid A (MPL), also increased the survival of mice infected with E. coli O18:K1. However, the dose of MPL required for optimal infection resistance was 100-fold greater than that of native, E. coli K-12 LPS, corresponding to the 100-fold reduced toxicity of MPL for mice and rabbits in lethality and pyrogenicity assays.
