A high degree of non-specific resistance to a lethal systemic infection was induced in mice by pretreatment with a small dose (>5 μUg/mouse) of the homologous lipopolysaccharide (LPS) or with heterologous rough-type LPS from 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 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 O18 :K1. However, the dose of MPL required for optimal infection resistance was 100-fold greater than that of native, K-12 LPS, corresponding to the 100-fold reduced toxicity of MPL for mice and rabbits in lethality and pyrogenicity assays.


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