Skip Navigation


International Immunology Advance Access originally published online on August 23, 2004
International Immunology 2004 16(10):1431-1437; doi:10.1093/intimm/dxh146
This Article
Right arrow Full Text Freely available
Right arrow FREE Full Text (PDF) Freely available
Right arrow All Versions of this Article:
16/10/1431    most recent
dxh146v1
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in ISI Web of Science
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Add to My Personal Archive
Right arrow Download to citation manager
Right arrow Search for citing articles in:
ISI Web of Science (37)
Right arrowRequest Permissions
Google Scholar
Right arrow Articles by Hashimoto, M.
Right arrow Articles by Ogawa, T.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Hashimoto, M.
Right arrow Articles by Ogawa, T.
Social Bookmarking
 Add to CiteULike   Add to Connotea   Add to Del.icio.us  
What's this?


© 2004 The Japanese Society for Immunology

Separation and structural analysis of lipoprotein in a lipopolysaccharide preparation from Porphyromonas gingivalis

Masahito Hashimoto, Yasuyuki Asai and Tomohiko Ogawa

Department of Oral Microbiology, Asahi University School of Dentistry, 1851-1 Hozumi, Mizuho, Gifu 501-0296, Japan

Correspondence to: T. Ogawa; E-mail: tomo527{at}dent.asahi-u.ac.jp

Lipopolysaccharide (LPS) preparations from the periodontopathic bacterium Porphyromonas gingivalis (Pg-LPS) are thought to require Toll-like receptor (TLR)2 rather than TLR4, a receptor of Escherichia coli LPS (Ec-LPS), for activation of immune cells. However, we previously reported that P. gingivalis lipid A, an immunostimulatory principal component of LPS, and its synthetic counterpart activate cells through a TLR4-dependent pathway but not via TLR2. In the present study, a lipoprotein from Pg-LPS (Pg-LP) was shown to be a principal component for TLR2-mediated cell activation. Pg-LP was separated by hydrophobic interaction chromatography followed by preparative electrophoresis and identified by internal peptide sequencing as PG1828, a putative lipoprotein encoded in the P. gingivalis genome. The N-terminal structure was characterized as a triacylated lipopeptide using mass spectrometry. Pg-LP, as well as Ec-LPS, was potent in inducing IL-8 production in human gingival fibroblasts. From our results, we propose that Pg-LP is a powerful inflammatory factor of P. gingivalis.

Keywords: Gram-negative bacteria, innate immunity, NF-{kappa}B activation, periodontal disease, Toll-like receptor

Transmitting editor: K. Sugamura


Add to CiteULike CiteULike   Add to Connotea Connotea   Add to Del.icio.us Del.icio.us    What's this?


This article has been cited by other articles:


Home page
JDRHome page
L. Kocgozlu, R. Elkaim, H. Tenenbaum, and S. Werner
Variable Cell Responses to P. gingivalis Lipopolysaccharide
Journal of Dental Research, August 1, 2009; 88(8): 741 - 745.
[Abstract] [Full Text] [PDF]


Home page
Pharmacol. Rev.Home page
L. A. J. O'Neill, C. E. Bryant, and S. L. Doyle
Therapeutic Targeting of Toll-Like Receptors for Infectious and Inflammatory Diseases and Cancer
Pharmacol. Rev., June 1, 2009; 61(2): 177 - 197.
[Abstract] [Full Text] [PDF]


Home page
J. Immunol.Home page
M. T.-H. Huang, D. J. Taxman, E. A. Holley-Guthrie, C. B. Moore, S. B. Willingham, V. Madden, R. K. Parsons, G. L. Featherstone, R. R. Arnold, B. P. O'Connor, et al.
Critical Role of Apoptotic Speck Protein Containing a Caspase Recruitment Domain (ASC) and NLRP3 in Causing Necrosis and ASC Speck Formation Induced by Porphyromonas gingivalis in Human Cells
J. Immunol., February 15, 2009; 182(4): 2395 - 2404.
[Abstract] [Full Text] [PDF]


Home page
Innate ImmunityHome page
M. Natsuka, A. Uehara, Shuhua Yang, S. Echigo, and H. Takada
A polymer-type water-soluble peptidoglycan exhibited both Toll-like receptor 2- and NOD2-agonistic activities, resulting in synergistic activation of human monocytic cells
Innate Immunity, October 1, 2008; 14(5): 298 - 308.
[Abstract] [PDF]


Home page
Innate ImmunityHome page
Diya Zhang, Lili Chen, Shenglai Li, Zhiyuan Gu, and Jie Yan
Lipopolysaccharide (LPS) of Porphyromonas gingivalis induces IL-1{beta}, TNF-{alpha} and IL-6 production by THP-1 cells in a way different from that of Escherichia coli LPS
Innate Immunity, April 1, 2008; 14(2): 99 - 107.
[Abstract] [PDF]


Home page
J. Immunol.Home page
M. Bastian, T. Braun, H. Bruns, M. Rollinghoff, and S. Stenger
Mycobacterial Lipopeptides Elicit CD4+ CTLs in Mycobacterium tuberculosis-Infected Humans
J. Immunol., March 1, 2008; 180(5): 3436 - 3446.
[Abstract] [Full Text] [PDF]


Home page
J. Immunol.Home page
Y. Asai, Y. Makimura, A. Kawabata, and T. Ogawa
Soluble CD14 Discriminates Slight Structural Differences between Lipid As That Lead to Distinct Host Cell Activation
J. Immunol., December 1, 2007; 179(11): 7674 - 7683.
[Abstract] [Full Text] [PDF]


Home page
Infect. Immun.Home page
M. Hashimoto, M. Furuyashiki, R. Kaseya, Y. Fukada, M. Akimaru, K. Aoyama, T. Okuno, T. Tamura, T. Kirikae, F. Kirikae, et al.
Evidence of Immunostimulating Lipoprotein Existing in the Natural Lipoteichoic Acid Fraction
Infect. Immun., April 1, 2007; 75(4): 1926 - 1932.
[Abstract] [Full Text] [PDF]


Home page
J Med MicrobiolHome page
Y. Asai, Y. Makimura, and T. Ogawa
Toll-like receptor 2-mediated dendritic cell activation by a Porphyromonas gingivalis synthetic lipopeptide
J. Med. Microbiol., April 1, 2007; 56(4): 459 - 465.
[Abstract] [Full Text] [PDF]


Home page
Cardiovasc ResHome page
C. Erridge, C. M. Spickett, and D. J. Webb
Non-enterobacterial endotoxins stimulate human coronary artery but not venous endothelial cell activation via Toll-like receptor 2
Cardiovasc Res, January 1, 2007; 73(1): 181 - 189.
[Abstract] [Full Text] [PDF]


Home page
J. Immunol.Home page
M. Hashimoto, K. Tawaratsumida, H. Kariya, A. Kiyohara, Y. Suda, F. Krikae, T. Kirikae, and F. Gotz
Not Lipoteichoic Acid but Lipoproteins Appear to Be the Dominant Immunobiologically Active Compounds in Staphylococcus aureus.
J. Immunol., September 1, 2006; 177(5): 3162 - 3169.
[Abstract] [Full Text] [PDF]


Home page
Int ImmunolHome page
M. Hashimoto, K. Tawaratsumida, H. Kariya, K. Aoyama, T. Tamura, and Y. Suda
Lipoprotein is a predominant Toll-like receptor 2 ligand in Staphylococcus aureus cell wall components
Int. Immunol., February 1, 2006; 18(2): 355 - 362.
[Abstract] [Full Text] [PDF]


Home page
J. Immunol.Home page
M.-A. Nahori, E. Fournie-Amazouz, N. S. Que-Gewirth, V. Balloy, M. Chignard, C. R. H. Raetz, I. Saint Girons, and C. Werts
Differential TLR Recognition of Leptospiral Lipid A and Lipopolysaccharide in Murine and Human Cells
J. Immunol., November 1, 2005; 175(9): 6022 - 6031.
[Abstract] [Full Text] [PDF]


Home page
Infect. Immun.Home page
G. Mancuso, A. Midiri, C. Biondo, C. Beninati, M. Gambuzza, D. Macri, A. Bellantoni, A. Weintraub, T. Espevik, and G. Teti
Bacteroides fragilis-Derived Lipopolysaccharide Produces Cell Activation and Lethal Toxicity via Toll-Like Receptor 4
Infect. Immun., September 1, 2005; 73(9): 5620 - 5627.
[Abstract] [Full Text] [PDF]


Home page
J. Immunol.Home page
G. Sen, A. Q. Khan, Q. Chen, and C. M. Snapper
In Vivo Humoral Immune Responses to Isolated Pneumococcal Polysaccharides Are Dependent on the Presence of Associated TLR Ligands
J. Immunol., September 1, 2005; 175(5): 3084 - 3091.
[Abstract] [Full Text] [PDF]


Home page
Infect. Immun.Home page
Y. Asai, M. Hashimoto, H. M. Fletcher, K. Miyake, S. Akira, and T. Ogawa
Lipopolysaccharide Preparation Extracted from Porphyromonas gingivalis Lipoprotein-Deficient Mutant Shows a Marked Decrease in Toll-Like Receptor 2-Mediated Signaling
Infect. Immun., April 1, 2005; 73(4): 2157 - 2163.
[Abstract] [Full Text] [PDF]


Home page
Int ImmunolHome page
K. Takeda and S. Akira
Toll-like receptors in innate immunity
Int. Immunol., January 1, 2005; 17(1): 1 - 14.
[Abstract] [Full Text] [PDF]



Disclaimer: Please note that abstracts for content published before 1996 were created through digital scanning and may therefore not exactly replicate the text of the original print issues. All efforts have been made to ensure accuracy, but the Publisher will not be held responsible for any remaining inaccuracies. If you require any further clarification, please contact our Customer Services Department.