C57BL/10/CR Mice: Nonresponders to Activation by the Lipid a Moiety of Bacterial Lipopolysaccharide
Open Access
- 1 January 1978
- journal article
- research article
- Published by Oxford University Press (OUP) in The Journal of Immunology
- Vol. 120 (1) , 249-253
- https://doi.org/10.4049/jimmunol.120.1.249
Abstract
C57BL/10/CR mice do not respond to the lipid A moiety of LPS. This defect was demonstrated in vivo by a decreased production of the acute phase serum amyloid protein SAA. In addition, the defect was demonstrated in vitro by using cultures of spleen cells and peritoneal cells. No mitogenesis of spleen cells or enhanced glucose utilization by either spleen cells or peritoneal cells was observed when the cells were stimulated by lipid A or phenol-extracted Escherichia coli K235 LPS. The response of these mice to PHA, Con A, Poly I:C, 8BrcGMP, and butanol extracted E. coli K235 LPS was normal. Thus, the inability of lipid A to stimulate B lymphocyte mitogenesis and activate peritoneal cells in vitro may correlate with its inability to induce the acute phase SAA in vivo. B10/CR mice represent another strain, similar to the C3H/HeJ, which is nonresponsive to lipid A and should be useful in elucidating the mechanism by which bacterial LPS activates cells.This publication has 4 references indexed in Scilit:
- Genetic defect in responsiveness to the B cell mitogen lipopolysaccharideEuropean Journal of Immunology, 1977
- Kinetics of serum amyloid protein A in casein-induced murine amyloidosis.Journal of Clinical Investigation, 1977
- Amyloid-Related Serum Protein SAA from Three Animal Species: Comparison with Human SAAThe Journal of Immunology, 1977
- Isolation of a lipid a bound polypeptide responsible for LPS- initiated mitogenesis of C3H/HeJ spleen cellsThe Journal of Experimental Medicine, 1976