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Infection and Immunity, April 2001, p. 2270-2276, Vol. 69, No. 4
0019-9567/01/$04.00+0   DOI: 10.1128/IAI.69.4.2270-2276.2001
Copyright © 2001, American Society for Microbiology. All rights reserved.

Micrococci and Peptidoglycan Activate TLR2right-arrow MyD88right-arrow IRAKright-arrow TRAFright-arrow NIKright-arrow IKKright-arrow NF-kappa B Signal Transduction Pathway That Induces Transcription of Interleukin-8

Qiuling Wang,1,dagger Roman Dziarski,1 Carsten J. Kirschning,2 Marta Muzio,3 and Dipika Gupta1,*

Northwest Center for Medical Education, Indiana University School of Medicine, Gary, Indiana 464081; Institute for Medical Microbiology, Immunology and Hygiene, Technical University of Munich, Munich, Germany2; and Department of Immunology and Cell Biology, Mario Negri Institute, I-20157 Milan, Italy3

Received 11 September 2000/Returned for modification 22 November 2000/Accepted 25 January 2001

This study was done to elucidate the signal transduction pathway of interleukin-8 (IL-8) induction by gram-positive bacteria. Bacteria (micrococci) and peptidoglycan (PGN) induced transcription of IL-8 in HEK293 cells expressing Toll-like receptor 2 (TLR2) and CD14 but not in those expressing TLR1 or TLR4. A mutation within the NF-kappa B site in the IL-8 promoter abrogated transcriptional induction of IL-8 by the two stimulants. Dominant negative myeloid differentiation protein (MyD88), IL-1 receptor-associated kinase (IRAK), NFkappa B-inducing kinase (NIK), and Ikappa B kinase (IKK) mutant forms completely inhibited micrococcus- and PGN-induced activation of NF-kappa B and expression of the gene for IL-8. Induction of NF-kappa B was partially inhibited by dominant negative tumor necrosis factor receptor-associated kinase 6 (TRAF6) but not TRAF2, whereas induction of IL-8 gene was partially inhibited by both TRAF6 and TRAF2. These data indicate that micrococci and PGN induce TLR2-dependent activation of the gene for IL-8 and that this activation requires MyD88, IRAK, NIK, IKK, and NF-kappa B and may also utilize TRAF6 and, to a lesser extent, TRAF2.

* Corresponding author. Mailing address: Northwest Center for Medical Education, Indiana University School of Medicine, 3400 Broadway, Gary, IN 46408. Phone: (219) 980-6557. Fax: (219) 980-6566. E-mail: dgupta{at}meded.iun.indiana.edu.

dagger Present address: Washington University School of Medicine, St. Louis, MO 63110.

Infection and Immunity, April 2001, p. 2270-2276, Vol. 69, No. 4
0019-9567/01/$04.00+0   DOI: 10.1128/IAI.69.4.2270-2276.2001
Copyright © 2001, American Society for Microbiology. All rights reserved.


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