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Published online before print December 27, 2007

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© by The Society for Leukocyte Biology
Journal of Leukocyte Biology, doi:10.1189/jlb.0607432

Received for publication June 26, 2007.
Revised November 8, 2007.
Accepted for publication November 20, 2007.

Article

Early and preferential induction of IL-1 receptor-associated kinase-M in THP-1 cells by LPS derived from Porphyromonas gingivalis

Hisanori Domon ^*, Tomoyuki Honda ^*, Taro Oda , Hiromasa Yoshie , and Kazuhisa Yamazaki ^*@

*Laboratory of Periodontology and Immunology, Department of Oral Health and Welfare, Niigata University Faculty of Dentistry, Division of Periodontology, Department of Oral Biological Science, Niigata University Graduate School of Medical Dental Sciences, and Center for Transdisciplinary Research, Niigata University, Niigata, Japan

^@ To whom correspondence should be addressed. E-mail: kaz{at}dent.niigata-u.ac.jp.

	Abstract

Abstract:

LPS of Porphyromonas gingivalis (P. gingivalis) is suggested to be a virulence factor in periodontitis, stimulating host cells to produce proinflammatory mediators. However, P. gingivalis LPS has been reported to show lower biological activity compared with Escherichia coli (E. coli) LPS. Although differences in the chemical structure of lipid A and the receptor conferring LPS signaling are thought to account for these characteristics, the precise reason is unknown. Here, we demonstrate that P. gingivalis LPS up-regulates IL-1R-associated kinase (IRAK)-M, a negative regulator of the TLR signaling pathway, in a THP-1-derived macrophage more robustly than E. coli LPS. Although down-regulation of IRAK-M by small interfering (si)RNA augmented transcription and translation of TNF-, IL-6, and IL-12 p40 in LPS-stimulated macrophages, the effect of siRNA was more prominent in P. gingivalis LPS-stimulated cells. Degradation of IRAK-1 was more obvious in E. coli LPS-stimulated macrophages than the cells stimulated with P. gingivalis LPS, suggesting that P. gingivalis LPS-induced IRAK-M suppressed dissociation of IRAK-1 from the receptor complex, resulting in escape from subsequent degradation. This activity may be involved in the chronic infection of this bacterium in periodontal tissue by serving as an escape mechanism from immune surveillance.

Key Words: human • monocytes/macrophages • signal transduction