Inheritance of lipopolysaccharide-enhanced nonspecific resistance to infection and of susceptibility to endotoxic shock in lipopolysaccharide low-responder mice.
In a previous study, we demonstrated that lipopolysaccharide (LPS) and other bacterial immunostimulants, in contrast to their activity in a closely related high-responder subline, failed to elicit nonspecific resistance in LPS low-responder mice against Klebsiella pneumoniae infection. To investigate the type of inheritance controlling the LPS-induced nonspecific resistance to infection, the present study was performed in low- and high-responder C3H sublines and in F1 and F2 hybrids. In addition, F1 mice were backcrossed to each parental type. Inheritance of susceptibility to endotoxin was also tested in both sublines and their hybrids and backcross progeny. For these latter assays, mice were previously adrenalectomized because removal of this gland considerably enhances their sensitivity. Our present findings are consistent with the hypothesis that LPS enhances nonspecific resistance to infection and that susceptibility to endotoxin shock in the absence of corticoids may be determined by a single autosomal dominant gene.
D000315:Adrenalectomy; D000818:Animals; D001770:Blood Bactericidal Activity; D003352:Corynebacterium / Q000276:immunology; D006824:Hybridization, Genetic; D007710:Klebsiella Infections / Q000150:complications / Q000235:genetics* / Q000517:prevention & control; D007928:Lethal Dose 50; D008070:Lipopolysaccharides; D051379:Mice; D008809:Mice, Inbred C3H; D008810:Mice, Inbred C57BL; D012772:Shock, Septic / Q000150:complications*
D008070:Lipopolysaccharides