Infection and Immunity, June 2001, p. 3663-3669, Vol. 69, No. 6
0019-9567/01/$04.00+0 DOI: 10.1128/IAI.69.6.3663-3669.2001
Copyright © 2001, American Society for Microbiology. All rights reserved.
-Inducing Ability
Department of Microbiology, Jichi Medical School, Tochigi 329-0498,1 and Department of Bacteriology, The Kitasato Institute, Tokyo 108-8642,2 Japan
Received 27 December 2000/Returned for modification 9 February 2001/Accepted 5 March 2001
Lipopolysaccharide (LPS) of Burkholderia cepacia was
purified by the conventional phenol-water extraction method
(preparation BcLPS-1), followed by enzymatic treatments with DNase,
RNase, trypsin, and proteinase K (preparation BcLPS-2), and finally by deoxycholate-phenol-water extraction (preparation BcLPS-3). Cells of
LPS-hyporesponsive C3H/HeJ mice were activated by both the BcLPS-1 and
the BcLPS-2 preparations but barely activated by BcLPS-3. When
LPS-responsive C3H/HeN mice were used as targets, endotoxic activities
such as lethal toxicity to galactosamine-sensitized mice, mitogenicity
to spleen cells, and activation of macrophages to induce tumor necrosis
factor alpha and interleukin-6 (IL-6) were strongly exhibited even by
highly purified BcLPS-3 at levels comparable to those of the highly
active enterobacterial LPS of Salmonella enterica serovar
Abortus-equi (SaeLPS), used as the control. The ability of BcLPS-3 to
activate murine macrophages for induction of IL-1
was, however, much
weaker than that of SaeLPS. Both accumulation of pro-IL-1
protein
and expression of IL-1
mRNA in macrophages by stimulation with
BcLPS-3 were much weaker than by stimulation with SaeLPS. These results
indicate that LPS of B. cepacia has the potential to play a
role as a pathogenic factor with strong activity comparable to that of
usual enterobacterial LPS, but unlike the latter, this LPS has a
relative lack of ability in the activation of murine macrophages to
induce IL-1
. The lack of IL-1
-inducing ability appears to be
caused by incomplete signal transduction somewhere in the upstream
step(s) of IL-1
gene transcription.
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