@article{mbs:/content/journal/jmm/10.1099/00222615-25-3-197, author = "Vuopio-Varkila, J. and Nurminen, Marjatta and Pyhälä, Liisa and Mäkelä, P. H.", title = "Lipopolysaccharide-induced non-specific resistance to systemic Escherichia coli infection in mice", journal= "Journal of Medical Microbiology", year = "1988", volume = "25", number = "3", pages = "197-203", doi = "https://doi.org/10.1099/00222615-25-3-197", url = "https://www.microbiologyresearch.org/content/journal/jmm/10.1099/00222615-25-3-197", publisher = "Microbiology Society", issn = "1473-5644", type = "Journal Article", abstract = "Summary. A high degree of non-specific resistance to a lethal systemic Escherichia coli infection was induced in mice by pretreatment with a small dose (< 5 μg/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.", }