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2. Assessment of the Plasma/Serum IgG Test to Screen for Periodontitis

Author

Kudo, C., primary, Naruishi, K., additional, Maeda, H., additional, Abiko, Y., additional, Hino, T., additional, Iwata, M., additional, Mitsuhashi, C., additional, Murakami, S., additional, Nagasawa, T., additional, Nagata, T., additional, Yoneda, S., additional, Nomura, Y., additional, Noguchi, T., additional, Numabe, Y., additional, Ogata, Y., additional, Sato, T., additional, Shimauchi, H., additional, Yamazaki, K., additional, Yoshimura, A., additional, and Takashiba, S., additional

Published
2012
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4. FGF-2 Stimulates Periodontal Regeneration

Author

Kitamura, M., primary, Akamatsu, M., additional, Machigashira, M., additional, Hara, Y., additional, Sakagami, R., additional, Hirofuji, T., additional, Hamachi, T., additional, Maeda, K., additional, Yokota, M., additional, Kido, J., additional, Nagata, T., additional, Kurihara, H., additional, Takashiba, S., additional, Sibutani, T., additional, Fukuda, M., additional, Noguchi, T., additional, Yamazaki, K., additional, Yoshie, H., additional, Ioroi, K., additional, Arai, T., additional, Nakagawa, T., additional, Ito, K., additional, Oda, S., additional, Izumi, Y., additional, Ogata, Y., additional, Yamada, S., additional, Shimauchi, H., additional, Kunimatsu, K., additional, Kawanami, M., additional, Fujii, T., additional, Furuichi, Y., additional, Furuuchi, T., additional, Sasano, T., additional, Imai, E., additional, Omae, M., additional, Watanuki, M., additional, and Murakami, S., additional

Published
2010
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5. Genetic Risk Factors for Periodontitis in a Japanese Population

Author

Kobayashi, T., primary, Nagata, T., additional, Murakami, S., additional, Takashiba, S., additional, Kurihara, H., additional, Izumi, Y., additional, Numabe, Y., additional, Watanabe, H., additional, Kataoka, M., additional, Nagai, A., additional, Hayashi, J., additional, Ohyama, H., additional, Okamatsu, Y., additional, Inagaki, Y., additional, Tai, H., additional, and Yoshie, H., additional

Published
2009
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6. α2 Integrin +807 Polymorphism in Drug-induced Gingival Overgrowth

Author

Ogino, M., primary, Kido, J., additional, Bando, M., additional, Hayashi, N., additional, Wada, C., additional, Nagata, T., additional, Nishimura, F., additional, Soga, Y., additional, Takashiba, S., additional, Kubota, T., additional, Itagaki, M., additional, Shimada, Y., additional, Tai, H., additional, Yoshie, H., additional, Yamazaki, N., additional, Shinohara, Y., additional, and Kataoka, M., additional

Published
2005
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14. Specific in situ visualization of plasma cells producing antibodies against Porphyromonas gingivalis in gingival radicular cyst: application of the enzyme-labeled antigen method.

Author

Tsuge S, Mizutani Y, Matsuoka K, Sawasaki T, Endo Y, Naruishi K, Maeda H, Takashiba S, Shiogama K, Inada K, and Tsutsumi Y

Subjects
Adult, Animals, Antigens, Bacterial chemistry, Antigens, Bacterial immunology, Bacterial Proteins chemistry, Bacterial Proteins immunology, Biotinylation, Female, Genes, Bacterial, Humans, Immunization, Lymph Nodes immunology, Lymph Nodes virology, Male, Middle Aged, Plasma Cells microbiology, Plasma Cells pathology, Porphyromonas gingivalis genetics, Radicular Cyst microbiology, Radicular Cyst pathology, Rats, Rats, Sprague-Dawley, Sensitivity and Specificity, Antibodies, Bacterial blood, Antigens, Bacterial metabolism, Bacterial Proteins metabolism, Endopeptidase K chemistry, Plasma Cells immunology, Porphyromonas gingivalis immunology, Radicular Cyst immunology
Abstract

The enzyme-labeled antigen method was applied to visualize plasma cells producing antibodies to Porphyromonas gingivalis, flora of the human oral cavity. Antibodies to P. gingivalis have reportedly been detected in sera of patients with periodontitis. Biotinylated bacterial antigens, Ag53, and four gingipain domains (Arg-pro, Arg-hgp, Lys-pro, and Lys-hgp) were prepared by the cell-free protein synthesis system using the wheat germ extract. In paraformaldehyde-fixed frozen sections of rat lymph nodes experimentally immunized with Ag53-positive and Ag53-negative P. gingivalis, plasma cells were labeled with biotinylated Arg-hgp and Lys-hgp. Antibodies to Ag53 were detected only in the nodes immunized with Ag53-positive bacteria. In two of eight lesions of gingival radicular cyst with inflammatory infiltration, CD138-positive plasma cells in frozen sections were signalized for Arg-hgp and Lys-hgp. An absorption study using unlabeled antigens confirmed the specificity of staining. The AlphaScreen method identified the same-type antibodies in tissue extracts but not in sera. Antibodies to Ag53, Arg-pro, and Lys-pro were undetectable. In two cases, serum antibodies to Arg-hgp and Lys-hgp were AlphaScreen positive, whereas plasma cells were scarcely observed within the lesions. These findings indicate the validity of the enzyme-labeled antigen method. This is the very first application of this novel histochemical technique to human clinical samples.

Published
2011
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15. High glucose up-regulates lipopolysaccharide-stimulated inflammatory cytokine production via c-jun N-terminal kinase in the monocytic cell line THP-1.

Author

Iwata H, Soga Y, Meguro M, Yoshizawa S, Okada Y, Iwamoto Y, Yamashita A, Takashiba S, and Nishimura F

Subjects
Cell Line, Tumor, Chemokine CCL2 genetics, Chemokine CCL5 genetics, Humans, Inflammation, Interleukin-1beta genetics, Interleukin-2, Monocytes, Oligonucleotide Array Sequence Analysis, Protein-Tyrosine Kinases genetics, Protein-Tyrosine Kinases metabolism, Tumor Necrosis Factor-alpha genetics, Cytokines biosynthesis, Cytokines genetics, Glucose pharmacology, JNK Mitogen-Activated Protein Kinases metabolism, Lipopolysaccharides pharmacology
Abstract

Diabetic subjects are susceptible to atherosclerosis. It has been postulated that inflammation plays a crucial role in atherogenesis. Since previous studies suggested persistent low-grade infection by Gram-negative bacteria such as Chlamydia spp. and/or periodontal infection is associated with increased atherogenesis among diabetic subjects, we hypothesized that macrophages under hyperglycemia respond to lipopolysaccharide (LPS) challenge in a more exaggerated manner than under normal glucose conditions. Therefore, we examined cytokine productivity and associated signal transduction molecules in LPS-stimulated the monocytic cell line THP-1, under conditions of hyperglycemia. Differentiated THP-1 cells were cultured under normal and high glucose conditions without fetal bovine serum, and were stimulated with Escherichia coli LPS in the presence of LPS binding protein. Following stimulation, activated signal transduction molecules were detected by protein microarray and confirmed thereafter. Results indicated that c-jun N-terminal kinase (JNK) was highly-phosphorylated at high glucose concentrations, and this was confirmed by Western-immunoblotting. Tumor necrosis factor-alpha and monocyte chemo-attractant protein-1 production were significantly enhanced under these conditions. SP600125, a selective inhibitor of JNK, dose-dependently suppressed the production of these cytokine. Therefore, we suggest that this may be one of the mechanisms by which sub-clinical infection by Gram-negative bacteria promotes atherosclerosis in diabetic subjects.

Published
2007
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