Damais C, Galelli A, Parant M
Ann Immunol (Paris). 1977 Jan-Mar;128(1-2):67-9.
In vitro and in vivo host reponses to lipopolysaccharide (LPS) and various immunostimulants were compared in C3h low-and highresponder mice, their F1, F2 and backcross hybrids. In contrast to the responsiveness of a congeneic high responder subline, LPS is unable to stimulate thymidine incorporation by splenocytes of the low-responder subline and to protect these mice against an unrelated bacterial infection, Moreover, although endotoxin extracted by trichloroacetic acid was mitogenic in these low-responder mice, it was still unable to increase their resistance against an infectious challenge; in addition, the LD50 of both endotoxin preparations was about 3,500 fold greater than in the high-responder mice. For this latter assay, mice were adrenaloctomized since it is well established that mouse's susceptibility to LPS is dramatically enhanced in the absence of glucocorticoids. Inheritance of susceptibility to lethal effect of endotoxin and of LPS-induced non-specific resistance to infection was also tested in both sublines, their hybrids and backcross progeny. The present findings are consistent with the hypothesis that these LPS host-responses may be determined by a single autosomal dominant gene.