Affiliation:
1. Division of Biology, Kansas State University, Manhattan, Kansas, USA
Abstract
We tested the D-galactosamine sensitization model with staphylococcal enterotoxin B (SEB). LPS was required for the lethal effects of SEB in D-galactosamine sensitized mice. Only two (2/62) among the C3HeB/FeJ (H-2k), Balb/c (H-2d) and C57BL/6J (H-2b) mice died in response to SEB in the absence of LPS whereas injection of SEB and minimally lethal concentrations of LPS became highly toxic. Similar to LPS, the lethal effect of SEB was dependent on the mouse strain used. Mouse strains more sensitive to the effects of LPS (Balb/c and C57BL/6J) were also more sensitive to the effects of SEB in comparison to C3H mice when equivalent doses of LPS and SEB were used. Among Balb/c and C3HeB/FeJ but not C57BL/6J mice, SEB (20 μg) potentiated the lethal effects of LPS at low doses (0.1 μg LPS), but had an apparent protective effect at high doses (1 μg LPS). Lastly, there was an inverse correlation between pathogenesis and serum IL-2 concentrations and splenic T cell activation in C3H mice. However, macrophage mobilization did correlate with lethality. Therefore, some questions remain about the mechanisms involved in the D-galactosamine/SEB pathogenesis model. We conclude that when sensitizing mice with D-galactosamine and assessing the lethal effects of SEB, endotoxin contamination must be assessed.
Subject
Infectious Diseases,Cell Biology,Molecular Biology,Immunology,Microbiology
Cited by
10 articles.
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