Lipopolysaccharide-induced non-specific resistance to systemic Escherichia coli infection in mice.
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.
Vuopio-Varkila
J
J
National Public Health Institute, Helsinki, Finland.
Nurminen
M
M
Pyhälä
L
L
Mäkelä
P H
PH
D000818:Animals; D004926:Escherichia coli / Q000276:immunology / Q000302:isolation & purification; D004927:Escherichia coli Infections / Q000276:immunology*; D005688:Galactosamine / Q000633:toxicity; D007110:Immunity, Active; D008070:Lipopolysaccharides / Q000276:immunology*; D051379:Mice; D008815:Mice, Inbred Strains; D013997:Time Factors
D008070:Lipopolysaccharides; D005688:Galactosamine