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Infection and Immunity, September 2000, p. 5026-5029, Vol. 68, No. 9
Department of Molecular Biology, Flanders
Interuniversity Institute for Biotechnology and University of
Ghent, B-9000 Ghent, Belgium
Received 24 February 2000/Returned for modification 24 April
2000/Accepted 15 June 2000
The proinflammatory cytokine tumor necrosis factor alpha (TNF-
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Copyright © 2000, American Society for Microbiology. All rights reserved.
The Major Acute-Phase Protein, Serum Amyloid P Component, in
Mice Is Not Involved in Endogenous Resistance against Tumor
Necrosis Factor Alpha-Induced Lethal Hepatitis, Shock, and
Skin Necrosis
)
induces lethal hepatitis when injected into
D-(+)-galactosamine-sensitized mice on the one hand or
systemic inflammatory response syndrome (SIRS) in normal
mice on the other hand. We studied whether serum amyloid P component
(SAP), the major acute-phase protein in mice, plays a
protective role in both lethal models. For this purpose, we used
SAP0/0 mice generated by gene targeting. We studied the
lethal response of SAP0/0 or SAP+/+ mice to
both lethal triggers but found no differences in the sensitivity of
both types of mice. We also investigated whether SAP is involved in
establishing two types of endogenous protection: one using a single
injection of interleukin-1
(IL-1) for desensitization and clearly
involving a liver protein, the other by tolerizing mice for 5 days
using small doses of human TNF-. Although after IL-1 or after
tolerization the SAP levels in the serum had risen fourfold in
the control mice and not in the SAP0/0 mice, the same
extents of desensitization and tolerization were achieved. Finally, we
observed that the induction of hemorrhagic necrosis in the skin of mice
by two consecutive local injections with TNF- was not altered in
SAP0/0 mice. We conclude that the presence or absence of
SAP has no influence on the sensitivity of mice to TNF--induced
hepatitis, SIRS, and hemorrhagic necrosis or on the endogenous
protective mechanisms of desensitization or tolerization.
*
Corresponding author. Mailing address: Department of
Molecular Biology, Flanders Interuniversity Institute for Biotechnology and University of Ghent, K. L. Ledeganckstraat 35, B-9000 Ghent, Belgium. Phone: 32-9-264-51-31. Fax: 32-9-264-53-48. E-mail:
claude{at}dmb.rug.ac.be.
Infection and Immunity, September 2000, p. 5026-5029, Vol. 68, No. 9
0019-9567/00/$04.00+0
Copyright © 2000, American Society for Microbiology. All rights reserved.
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