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Infection and Immunity, March 2000, p. 1600-1607, Vol. 68, No. 3
0019-9567/00/$04.00+0
Copyright © 2000, American Society for Microbiology. All rights reserved.

Bacterial Induction of Beta Interferon in Mice Is a Function of the Lipopolysaccharide Component

Andreas Sing,1,dagger Thomas Merlin,1 Hans-Peter Knopf,1,Dagger Peter J. Nielsen,1 Harald Loppnow,2 Chris Galanos,1 and Marina A. Freudenberg1,*

Max-Planck-Institut für Immunbiologie, D-79108 Freiburg,1 and Klinik und Poliklinik für Innere Medizin III, Forschungslabor, D-06097 Halle (Saale),2 Germany

Received 22 July 1999/Returned for modification 20 September 1999/Accepted 22 November 1999

We investigated the reason for the inability of lipopolysaccharide (LPS)-resistant (Lps-defective [Lpsd]) C57BL/10ScCr mice to produce beta interferon (IFN-beta ) when stimulated with bacteria. For this purpose, the IFN-beta and other macrophage cytokine responses induced by LPS and several killed gram-negative and gram-positive bacteria in LPS-sensitive (Lps-normal [Lpsn]; C57BL/10ScSn and BALB/c) and Lpsd (C57BL/10ScCr and BALB/c/l) mice in vitro and in vivo were investigated on the mRNA and protein levels. In addition, double-stranded RNA (dsRNA) was used as a nonbacterial stimulus. LPS and all gram-negative bacteria employed induced IFN-beta in the Lpsn mice but not in the Lpsd mice. All gram-positive bacteria tested failed to induce significant amounts of IFN-beta in all four of the mouse strains used. As expected, all other cytokines tested (tumor necrosis factor alpha, interleukin 1alpha [IL-1alpha ], IL-6, and IL-10) were differentially induced by gram-negative and gram-positive bacteria. Stimulation with dsRNA induced IFN-beta and all other cytokines mentioned above in all mouse strains, regardless of their LPS sensitivities. The results suggest strongly that LPS is the only bacterial component capable of inducing IFN-beta in significant amounts that are readily detectable under the conditions used in this study. Consequently, in mice, IFN-beta is inducible only by gram-negative bacteria, but not in C57BL/10ScCr or other LPS-resistant mice.

* Corresponding author. Mailing address: Max-Planck-Institut für Immunbiologie, Stübeweg 51, D-79108 Freiburg, Germany. Phone: 49-761-5108-404. Fax: 49-761-5108-403. E-mail: freudenberg{at}immunbio.mpg.de.

dagger Present address: Max-von-Pettenkofer-Institut für Mikrobiologie und Hygiene, Abt. Bakteriologie, D-80336 Munich, Germany.

Dagger Present address: Novartis Pharma AG, Biotechnology, S-506.3.14, CH-4002 Basel, Switzerland.

Infection and Immunity, March 2000, p. 1600-1607, Vol. 68, No. 3
0019-9567/00/$04.00+0
Copyright © 2000, American Society for Microbiology. All rights reserved.


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