Immunologic responsiveness of the C3H/HeJ mouse: differential ability of butanol-extracted lipopolysaccharide (LPS) to evoke LPS-mediated effects.

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Abstract
The LPS-protein complex extracted from the cell wall of Escherichia coli K235 by the butanol-water technique was shown to evoke a mitogenic response in bone marrow-derived (B) lymphocytes from the C3H/HeJ mouse strain. These mice are resistant to the effects of LPS extracted with phenol. The ability of butanol-extracted LPS to modulate a spectrum of C3H/HeJ B-cell functions was investigated. Butanol-extracted (LPS-B) and phenol-extracted (LPS-P) LPS preparations activated responder C3H/St spleen cell cultures to polyclonal antibody production. Only LPS-B activated C3H/HeJ spleen cells. LPS-P and LPS-B acted as adjuvants when injected after aggregated human .gamma. globulin (HGG) in C3H/St mice. Neither preparation was effective as an adjuvant in C3H/HeJ mice. LPS-P injected with deaggregated HGG (tolerogen) into LPS-sensitive mice was shown previously to inhibit the induction of tolerance to HGG. LPS-B, but not LPS-P, was able to inhibit tolerance induction to HGG in the C3H/HeJ. Both preparations were effective in the C3H/St. LPS was shown to bypass tolerant T [thymus derived] cells in LPS-sensitive mice late in tolerance to HGG at a time when B cells are responsive. In the C3H/HeJ, LPS-B and LPS-P were not capable of this function. The responsiveness of these B cells to HGG was demonstrated in transfer experiments. In the C3H/HeJ, LPS-B stimulates mitogenesis, polyclonal B-cell activation and inhibition of tolerance induction, but cannot act as an effective adjuvant or as a bypass mechanism to activate B cells in the presence of tolerant T cells. The explanation for this pattern of responses may be attributable to yet another cellular defect in the C3H/HeJ mouse.

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