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Originally published In Press as doi:10.1074/jbc.M208140200 on September 27, 2002

J. Biol. Chem., Vol. 277, Issue 49, 47444-47450, December 6, 2002
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Inhibition of p38 MAPK by Glucocorticoids via Induction of MAPK Phosphatase-1 Enhances Nontypeable Haemophilus influenzae-induced Expression of Toll-like Receptor 2*

Akira ImasatoDagger , Christéle Desbois-Mouthon§, Jiahuai Han, Hirofumi Kai||, Andrew C. B. Cato**, Shizuo AkiraDagger Dagger , and Jian-Dong LiDagger §§

From the Dagger  Gonda Department of Cell and Molecular Biology, House Ear Institute, and the Department of Otolaryngology, University of Southern California, Los Angeles, California 90057, § INSERM U-402, Faculté de Médecine Saint-Antoine, Paris 75571, France, the  Department of Immunology, the Scripps Research Institute, La Jolla, California 92037, the || Department of Molecular Medicine, Kumamoto University, Kumamoto 862-0973, Japan, the ** Forschungszentrum Karlsruhe, Institute of Toxicology & Genetics, P. O. Box 3640, Karlsruhe D-76021, Germany, the Dagger Dagger  Department of Host Defense, Research Institute for Microbial Diseases, Osaka University, Core Research for Evolutional Science and Technology of Japan Science and Technology Corporation, 3-1 Yamada-oka, Suita, Osaka 565-0871, Japan

Despite the importance of glucocorticoids in suppressing immune and inflammatory responses, their role in enhancing host immune and defense response against invading bacteria is poorly understood. We have demonstrated recently that glucocorticoids synergistically enhance nontypeable Haemophilus influenzae (NTHi)-induced expression of Toll-like receptor 2 (TLR2), an important TLR family member that has been shown to play a critical role in host immune and defense response. However, the molecular mechanisms underlying the glucocorticoid-mediated enhancement of TLR2 induction still remain unknown. Here we show that glucocorticoids synergistically enhance NTHi-induced TLR2 expression via specific up-regulation of the MAPK phosphatase-1 (MKP-1) that, in turn, leads to dephosphorylation and inactivation of p38 MAPK, the negative regulator for TLR2 expression. Moreover, increased expression of TLR2 in epithelial cells greatly enhances the NTHi-induced expression of several key cytokines, including tumor necrosis factor-alpha and interleukins 1beta and 8, thereby contributing significantly to host immune and defense response. These studies may bring new insights into the novel role of glucocorticoids in orchestrating and optimizing host immune and defense responses during bacterial infections and enhance our understanding of the signaling mechanisms underlying the glucocorticoid-mediated attenuation of MAPKs.

* This work was supported by National Institutes of Health Grants DC04562 (to J. D. L.) and AI41637 (to J. H.).The costs of publication of this article were defrayed in part by the payment of page charges. The article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.

§§ To whom correspondence should be addressed: the Gonda Dept. of Cell and Molecular Biology, House Ear Institute, University of Southern California, 2100 West Third St., Los Angeles, CA 90057. Tel.: 213-273-8083; Fax: 213-273-8088; E-mail: jdli@hei.org.

Copyright © 2002 by The American Society for Biochemistry and Molecular Biology, Inc.
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