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Infection and Immunity, April 2004, p. 2131-2139, Vol. 72, No. 4
0019-9567/04/$08.00+0     DOI: 10.1128/IAI.72.4.2131-2139.2004
Copyright © 2004, American Society for Microbiology. All Rights Reserved.

Toll-Like Receptor 2 Is Required for Optimal Control of Listeria monocytogenes Infection

David Torres,1 Mathieu Barrier,1 Franck Bihl,1 Valerie J. F. Quesniaux,1 Isabelle Maillet,1 Shizuo Akira,2 Bernhard Ryffel,1* and François Erard1

CNRS, Laboratoire de Génétique expérimentale et moléculaire (GEM2358), F-45071 Orléans Cedex 2, France,1 Department of Host Defense, Research Institute for Microbial Diseases, Osaka University, 3-1 Yamada-oka, Suita, Osaka 565-0871, Japan2

Received 12 November 2003/ Returned for modification 25 November 2003/ Accepted 24 December 2003

The control of Listeria monocytogenes infection depends on the rapid activation of the innate immune system, likely through Toll-like receptors (TLR), since mice deficient for the common adapter protein of TLR signaling, myeloid differentiation factor 88 (MyD88), succumb to Listeria infection. In order to test whether TLR2 is involved in the control of infections, we compared the host response in TLR2-deficient mice with that in wild-type mice. Here we show that TLR2-deficient mice are more susceptible to systemic infection by Listeria than are wild-type mice, with a reduced survival rate, increased bacterial burden in the liver, and abundant and larger hepatic microabscesses containing increased numbers of neutrophils. The production of tumor necrosis factor, interleukin-12, and nitric oxide and the expression of the costimulatory molecules CD40 and CD86, which are necessary for the control of infection, were reduced in TLR2-deficient macrophages and dendritic cells stimulated by Listeria and were almost abolished in the absence of MyD88, coincident with the high susceptibility of MyD88-deficient mice to in vivo infection. Therefore, the present data demonstrate a role for TLR2 in the control of Listeria infection, but other MyD88-dependent signals may contribute to host resistance.

* Corresponding author. Mailing address: Génétique expérimentale et moléculaire (GEM2358), Institut de Transgénose, CNRS, 3B rue de la Férollerie, F-45071 Orléans Cedex 2, France. Phone: 33 238 25 5439. Fax: 33 238 25 7979. E-mail: bryffel{at}cnrs-orleans.fr.

Editor: F. C. Fang

Infection and Immunity, April 2004, p. 2131-2139, Vol. 72, No. 4
0019-9567/04/$08.00+0     DOI: 10.1128/IAI.72.4.2131-2139.2004
Copyright © 2004, American Society for Microbiology. All Rights Reserved.



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