title: Hyporesponsiveness of inflamed human gingival fibroblasts from patients with chronic periodontal diseases against cell surface components of Porphyromonas gingivalis.
abstract: Inflamed human gingival fibroblasts (HGF) of patients with chronic periodontal diseases have less active interleukin-8 (IL-8) production compared with normal HGF of volunteers with healthy gingival tissues, after stimulation with Porphyromonas gingivalis surface components such as fimbriae, lipopolysaccharide (LPS) and its lipid A, but not LPS or lipid A from other bacterial species. A decrease in number of specific binding sites for P. gingivalis fimbrial molecules in inflamed HGF is also observed by Scatchard plot analysis. A short exposure (6 h) to P. gingivalis LPS resulted in significant potentiation of the LPS-dependent IL-8 production in normal HGF, whereas a long exposure (48 h) to the LPS significantly reduced IL-8 production. Tyrosine phosphorylation of proteins of 127 kDa and 186 kDa in inflamed HGF stimulated with P. gingivalis fimbriae or its LPS was observed by immunoblotting, and these two phosphoproteins were termed tolerance-induced protein, TIP. Protein bands of 45 kDa which bound to radioiodinated P. gingivalis fimbriae in the presence and absence of fetal bovine serum (FBS), and major 73-kDa and minor 30-kDa and 45-kDa bands which bound to radioiodinated P. gingivalis LPS in the presence of FBS in normal and inflamed HGF were observed by using photocrosslinking. These findings suggest that the hyporesponsiveness of HGF induced by a prolonged exposure to P. gingivalis may emerge because of HGF damage or result from host defense in chronic periodontal lesions.
authors.affiliation: Department of Oral Microbiology, Osaka University Faculty of Dentistry, Suita, Japan.
authors.forename: T
authors.initials: T
authors.lastname: Ogawa
authors.forename: A
authors.initials: A
authors.lastname: Ozaki
authors.forename: H
authors.initials: H
authors.lastname: Shimauchi
authors.forename: H
authors.initials: H
authors.lastname: Uchida
mesh_terms: D000328:Adult; D001426:Bacterial Proteins / Q000138:chemical synthesis / Q000494:pharmacology; D016227:Benzoquinones; D015153:Blotting, Western; D002478:Cells, Cultured; D002908:Chronic Disease; D004791:Enzyme Inhibitors / Q000494:pharmacology; D005347:Fibroblasts / Q000166:cytology / Q000276:immunology; D010861:Fimbriae, Bacterial / Q000276:immunology; D005881:Gingiva / Q000166:cytology / Q000276:immunology*; D005891:Gingivitis / Q000276:immunology*; D006801:Humans; D016209:Interleukin-8 / Q000096:biosynthesis*; D047029:Lactams, Macrocyclic; D010455:Peptides / Q000138:chemical synthesis / Q000494:pharmacology; D010518:Periodontitis / Q000276:immunology* / Q000473:pathology; D016966:Porphyromonas gingivalis / Q000276:immunology*; D011505:Protein-Tyrosine Kinases / Q000037:antagonists & inhibitors; D011809:Quinones / Q000494:pharmacology; D017828:Rifabutin / Q000031:analogs & derivatives
chemical_list: D001426:Bacterial Proteins; D016227:Benzoquinones; D004791:Enzyme Inhibitors; D016209:Interleukin-8; D047029:Lactams, Macrocyclic; D010455:Peptides; D011809:Quinones; D017828:Rifabutin; C020754:herbimycin; D011505:Protein-Tyrosine Kinases