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Haloacid dehalogenase (HAD) family phosphatases are widespread in prokaryotes and are generally involved in metabolic processes. Porphyromonas gingivalis, an invasive periodontal pathogen, secretes the HAD family phosphoserine phosphatase SerB653 when in contact with gingival epithelial cells. Here we characterize the structure and enzymatic activity of SerB653 and show that a SerB653 allelic replacement mutant of P. gingivalis is deficient in internalization and persistence in gingival epithelial cells. In contrast, mutation of a second HAD family serine phosphatase of P. gingivalis (SerB1170), or of a serine transporter, did not affect invasion. A pull-down assay identified GAPDH and heat-shock protein 90 as potential substrates for SerB653. Furthermore, exogenous phosphatase regulated microtubule dynamics in host cells. These data indicate that P. gingivalis has adapted a formerly metabolic enzyme to facilitate entry into host cells by modulating host cytoskeletal architecture. Our findings define a virulence-related role of a HAD family phosphatase and reveal an invasin of an important periodontal pathogen. bacterial pathogenesis | invasin | microtubules | intracellular survival

A study of the use of an essential oil containing mouthrinse in reducing plaque and gingivitis in patients who brush and floss regularly is presented. The results show that the use of an adjunctive like essential oil containing mouthrinse helps in reducing plaque and gingivitis in patients who brush and floss regularly.

Byline: K. Noguchi (1), K. Iwasaki (1), I. Ishikawa (1) Abstract: In the present study, the effect of prostaglandin E.sub.2 (PGE.sub.2) on intercellular adhesion molecule-1 (ICAM-1) expression in interferon-I3 (IFN-I3)-stimulated human gingival fibroblasts (HGF) was investigated. Addition of PGE.sub.2 to HGF inhibited ICAM-1 expression elicited by IFN-I3. As PGE.sub.2 elevated intercellular cyclic AMP (cAMP) levels in HGF in a dose-dependent fashion, the effect of dibutyryl cAMP and 8-bromo-cAMP, cAMP analogues, on IFN-I3-elicited ICAM-1 expression was examined. Both the agents downregulated ICAM-1 expression in IFN-I3-stimulated HGF. Next, we examined which subtype(s) of the four PGE.sub.2 receptor subtypes (EP.sub.1, EP.sub.2, EP.sub.3 and EP.sub.4) modulated the ICAM-1 expression elicited by IFN-I3, using subtype-specific agonists or antagonists. An EP.sub.2/EP.sub.4 agonist, 11-deoxy-PGE.sub.1, attenuated IFN-I3-elicited ICAM-1 expression in a concentration-dependent manner. A specific EP.sub.4 antagonist, AH-23848B, showed no effect on inhibition of IFN-I3-elicited ICAM-1 expression by PGE.sub.2 and 11-deoxy-PGE.sub.1. Butaprost, an EP.sub.2-selective agonist, mimicked inhibition of IFN-I3-elicited ICAM-1 expression by 11-deoxy-PGE.sub.1. An EP.sub.3 agonist, ONO-AP-324, was inert with respect to IFN-I3-elicited ICAM-1 expression. Sulprostone, an EP.sub.1/EP.sub.3 agonist, showed stimulatory effect on ICAM-1 expression elicited by IFN-I3. From these results, we suggest that PGE.sub.2 downregulates IFN-I3-induced ICAM-1 expression in HGF, primarily via EP.sub.2 receptors by cAMP-dependent signaling pathways. Author Affiliation: (1) Department of Periodontology, Graduate School, Faculty of Dentistry, Tokyo Medical and Dental University, 1--5--45, Yushima, Bunkyo-ku, Tokyo, 113--8549, Japan Article History: Registration Date: 30/09/2004

Byline: Noriko Sugita (1), Asako Kimura (1,2), Yutaka Matsuki (1), Tadashi Yamamoto (2), Hiromasa Yoshie (1), Kohji Hara (1) Abstract: DNA binding activity of NF-IoB and AP-1 were examined in neutrophils stimulated with LPS purified from P. gingivalis, a major pathogenic bacteria of periodontitis lesion. Porphyromonas gingivalis LPS enhanced the activity reaching a peak at a concentration of 500 ng/ml in the absence of serum. The NF-IoB activation stimulated with 10 ng/ml of P. gingivalis LPS was suppressed approximately 44% by treatment of neutrophils with anti-CD14 antibody under the presence of serum. Increase in the steady-state IL-8 mRNA level was concomitantly observed by stimulation of neutrophils with 500 ng/ml of P. gingivalis LPS under the absence of serum. These results indicate that P. gingivalis LPS activates NF-IoB and AP-1 in both serum-dependent and -independent manners, followed by increased IL-8 transcription in neutrophils, and suggested a role for P. gingivalis LPS in IL-8 synthesis by neutrophils in inflamed gingiva and GCF. Author Affiliation: (1) Department of Periodontology, Niigata University School of Dentistry, Japan (2) Institute of Nephrology, Niigata University School of Medicine, Japan Article History: Registration Date: 03/10/2004

The anaerobic gram-negative rod bacterium porphyromona gingivalis is an etiological agent in chronic adult peridontal disease. Its proteases show a complicated pattern of enzymes, and studies with p. gingivalis W50 have show that the Arg-x activity consists of Ri, RiA and RIB, derived from prpR1. Southern hybridization confirmed the genomic organization of prpR1,

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