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Lipoteichoic Acid Isolated from Lactobacillus plantarum Inhibits Lipopolysaccharide-Induced TNF- Production in THP-1 Cells and Endotoxin Shock in Mice¹

Han Geun Kim^*,, Na-Ra Kim^*, Min Geun Gim^*, Jung Min Lee^*,, Seung Yeon Lee^*, Mi Yeon Ko^*, Joo Yun Kim, Seung Hyun Han and Dae Kyun Chung^2,*,

^* Graduate School of Biotechnology and Institute of Life Science and Resources, Kyung Hee University, Yongin, Korea; Skin Biotechnology Center, Kyung Hee University, Yongin, Korea; Division of Cardiology, Samsung Medical Center and Samsung Biomedical Research Institute, School of Medicine, Sungkyunkwan University, Seoul, Korea; and Laboratory of Microbial Infection and Immunology, School of Dentistry, Seoul National University, Seoul, Korea

In this study, the effect of Lactobacillus plantarum lipoteichoic acid (pLTA) on LPS-induced MAPK activation, NF-B activation, and the expression of TNF- and IL-1R-associated kinase M (IRAK-M) was examined. The expression of the pattern recognition receptor and the survival rate of mice were also examined. pLTA pretreatment inhibited the phosphorylation of ERK, JNK, and p38 kinase. It also inhibited the degradation of IB and IBβ, as well as the activation of the LPS-induced TNF- factor in response to subsequent LPS stimulation. These changes were accompanied by the suppression of the LPS-induced expression of TLR4, NOD1, and NOD2, and the induction of IRAK-M, with a concurrent reduction of TNF- secretion. Furthermore, the overexpression of pattern recognition receptors such as TLR4, NOD1, and NOD2 and the degradation of IRAK-M by transient transfection were found to reinstate the production of TNF- after LPS restimulation. In addition, the i.p. injection of pLTA suppressed fatality, and decreased the level of TNF- in the blood, in LPS-induced endotoxin shock mice. In conclusion, these data extend our understanding of the pLTA tolerance mechanism, which is related to the inhibition of LPS-induced endotoxin shock, and suggest that pLTA may have promise as a new therapeutic agent for LPS-induced septic shock.

The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked advertisement in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.

¹ This work was supported by the 21C Frontier Microbial Genomics and Application Center Program, Ministry of Science and Technology (Grant MG05-0307-2-0), Republic of Korea.

² Address correspondence and reprint requests to Dr. Dae Kyun Chung, Graduate School of Biotechnology and Institute of Life Science and Resources, Kyung Hee University, Yongin, Korea, 449-701. E-mail address: dkchung{at}khu.ac.kr

³ Abbreviations used in this paper: LTA, lipoteichoic acid; PGN, peptidoglycan; pLTA, L. plantarum lipoteichoic acid; PRR, pattern recognition receptor; BMM, bone marrow-derived macrophage; LITAF, LPS-induced TNF- factor; AST, aspartate aminotransferase; ALT, alanine aminotransferase; aLTA, S. aureus LTA; CX, crude extract; CW, cell wall; TA, teichoic acid; sup, supernatant; aPGN, S. aureus PGN; IRAK-M, IL-1R-associated kinase M; siRNA, small interference RNA.