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Lps Gene Regulation of Mucosal Immunity and Susceptibility to Salmonella Infection in Mice

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Genetic Control of the Susceptibility to Bacterial Infection

Part of the book series: Current Topics in Microbiology and Immunology ((CT MICROBIOLOGY,volume 124))

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Abstract

In 1940, Hill and coworkers reported that the inoculation of a heterogeneous population of mice with endotoxin, followed by the selective interbreeding of survivors, produced a strain of mice which displayed significantly increased resistance to the lethal effects of endotoxin. This finding suggested that the degree of sensitivity to endotoxin challenge was a heritable trait in mice. The demonstration by Sultzer (1968) that inbred C3H/HeJ mice were resistant to the endotoxin-induced infiltration of mononuclear cells into the peritoneal cavity, as well as to the toxicity of endotoxin, identified this mouse strain as a valuable tool for the study of mechanisms of resistance to endotoxin toxicity and genetic control of murine sensitivity to endotoxin. By analyzing the LPS responsiveness of 11 different mouse strains which were derived from the C3H strain between 1920 and 1968, Glode and Rosenstreich (1976) traced the chronology of mutational events which led to the defect in LPS responsiveness of C3H/HeJ mice. The unresponsiveness of C3H/HeJ mice to LPS was reported to be caused by a genetic mutation which occurred some time between 1960 and 1965 and was inbred into the C3H/HeJ line by 1968 (Glode and Rosenstreich 1976; reviewed by Vogel et al. 1979).

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Colwell, D.E., Michalek, S.M., McGhee, J.R. (1986). Lps Gene Regulation of Mucosal Immunity and Susceptibility to Salmonella Infection in Mice. In: Briles, D.E. (eds) Genetic Control of the Susceptibility to Bacterial Infection. Current Topics in Microbiology and Immunology, vol 124. Springer, Berlin, Heidelberg. https://doi.org/10.1007/978-3-642-70986-9_8

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  • DOI: https://doi.org/10.1007/978-3-642-70986-9_8

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