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Division of Microbiology, National Institute of Health Sciences, Tokyo, Japan
The stimulation of both THP-1 and U937 human-derived cells by
Salmonella lipid A preparations from various strains, as
assessed by TNF-
induction and NF-
B activation, was found to be
very low (almost inactive) compared with Escherichia
coli lipid A, but all of the lipid As exerted strong activity
on mouse cells and on Limulus gelation activity.
Experiments using chemically synthesized E. coli-type
hexaacylated lipid A (506) and Salmonella-type
heptaacylated lipid A (516) yielded clearer results. Both lipid A
preparations strongly induced TNF- release and activated NF-B in
mouse peritoneal macrophages and mouse macrophage-like cell line J774-1
and induced Limulus gelation activity, although the
activity of the latter was slightly weaker than that of the former.
However, 516 was completely inactive on both THP-1 and U937 cells in
terms of both induction of TNF- and NF-B activation, whereas 506
displayed strong activity on both cells, the same as natural E.
coli LPS. In contrast to the action of the lipid A
preparations, all the Salmonella LPSs also exhibited
full activity on human cells. However, the polysaccharide portion of
the LPS neither exhibited TNF- induction activity on the cells when
administered alone or together with lipid A nor inhibited the activity
of the LPS. These results suggest that the mechanism of activation by
LPS or the recognition of lipid A structure by human and mouse cells
may differ. In addition, both 516 and lipid A from
Salmonella were found to antagonize the 506 and
E. coli LPS action that induced TNF- release and
NF-B activation in THP-1 cells.
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