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An early report: a modified porphyrin-linked metronidazole targeting intracellular porphyromonas gingivalis in cultured oral epithelial cells

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International Journal of Oral Science 2017年第3期9卷 167-173页

作者： Ping Ye Jiho Chang Lin Feng Foo Benjamin C-M Yap Institute of Dental Research Centre for Oral Health Westmead Hospital Affiliation of Faculty of Dentistry the University of Sydney

porphyromonas gingivalis （P. gingivalis） has a strong association with the pathogenesis of periodontal disease. Recurrence of periodontal disease following therapy is attributed to numerous factors, and of growing interest is the potential problem of intracellular bacteria that are able to persist and multiply within the host cell, thereby facilitating relapse of infection. The effect of antibiotic therapy in controlling P. gingivalis is questionable. Accordingly, while metronidazole is very effective against anaerobic extracellular P. gingivalis by disrupting the DNA of anaerobic microbial cells, this antibiotic does not effectively penetrate into mammalian cells to inhibit intracellular bacteria. Therefore in the present study, a modified porphyrin-linked metronidazole adducts, developed in our laboratory, was used to kill intracellular P. gingivalis. A series of experiments were performed, including cytotoxicity assays and cellular uptake of adducts by flow cytometry coupled with live cell imaging analysis, P. gingivalis invasion and elimination assays, and the analysis of colocalization of P. gingivalis and porphyrin-linked metronidazole by confocal laser scanning microscopy. Findings indicated that P. gingivalis and porphyrin-linked metronidazole were colocalized in the cytoplasm, and this compound was able to kill P. gingivalis intracellular with a sufficient culture time. This is a novel antimicrobial approach in the elimination of P. gingivalis from the oral cavity.

关键词： porphyrin-linked metronidazole porphyromonas gingivalis periodontitis oral epithelial cells

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Characterization of Fusobacterium nucleatum ATCC 23726 adhesins involved in strain-specific attachment to porphyromonas gingivalis

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International Journal of Oral Science 2016年第3期8卷 138-144页

作者： Jane Park Bhumika Shokeen Susan K Haake Renate Lux School of Dentistry University of California at Los Angeles Los Angeles USA

Bacterial adherence is an essential virulence factor in pathogenesis and infection. Fusobacterium nucleatum has a central role in oral biofilm architecture by acting as a bridge between early Gram-positive and late Gram-negative colonizers that do not otherwise adhere to each other. In this study, we survey a key adherence interaction of F. nucleatum with porphyromonas gingivalis, and present evidence that multiple fusobacterial adhesins have a role in the attachment of F. nucleatum ATCC 23726 to P. gingivalis in a highly strain-dependent manner. Interaction between these species displayed varying sensitivities to arginine, galactose and lactose. Arginine was found to hamper coaggregation by at least 62% and up to 89% with several P. gingivalis strains and galactose inhibition ranged from no inhibition up to 58% with the same P. gingivalis strains. Lactose consistently inhibited F. nucleatum interaction with these P. gingivalis strains ranging from 40% to 56% decrease in coaggregation. Among the adhesins involved are the previously described Fap2 and surprisingly, RadD, which was described in an earlier study for its function in attachment of F. nucleatum to Gram-positive species. We also provide evidence for the presence of at least one additional adhesin that is sensitive to arginine but unlike Fap2 and RadD, is not a member of the autotransporter family type of fusobacterial large outer membrane proteins. The strain-specific binding profile of multiple fusobacterial adhesins to P. gingivalis highlights the heterogeneity and complexity of interspecies interactions in the oral cavity.

关键词： adhesin bio?lm coaggregation Fusobacterium nucleatum porphyromonas gingivalis

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Analysis of differential expression of tight junction proteins in cultured oral epithelial cells altered by porphyromonas gingivalis,porphyromonas gingivalis lipopolysaccharide,and extracellular adenosine triphosphate

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International Journal of Oral Science 2017年第4期9卷 238-244页

作者： wei guo peng wang zhong-hao liu ping ye department of endodontics yantai stomatological hospitalbinzhou medical universityYantaiChina department of pediatrics yantai stomatological hospitalbinzhou medical universityYantaiChina department of implant yantai stomatological hospitalbinzhou medical universityYantaiChina institute of dental research centre for oral healthwestmead hospitalWestmeadAustralia faculty of dentistry the university of sydneySydneyAustralia

Tight junctions （TJs） are the most apical intercellular junctions of epithelial cells formed by occludin, claudins, junctional adhesion molecules （JAMs）, and zonula occludens （ZO）. Tight junction proteins can sense the presence of bacteria and regulate the transcription of target genes that encode effectors and regulators of the immune response. The aim of this study was to determine the impact of TJ proteins in response to porphyromonas gingivalis （P. gingivalis）, P. gingivalis lipopolysaccharide （P. gingivalis LPS）, and extracellular adenosine triphosphate （ATP） in the oral epithelial cell culture model. Quantified real time- polymerase chain reaction （RT-PCR）, immunoblots, and immunostaining were performed to assess the gene and protein expression in TJs. It was found that P. gingivalis infection led to transient upregulation of the genes encoding occludin, claudin- 1, and claudin-4 but not JAM-A, claudin-15, or ZO-1, while P. gingivalis LPS increased claudin-1, claudin-15, and ZO-1 and decreased occludin, JAM-A, and claudin-4. Tight junction proteins showed significant upregulation in the above two groups when cells were pretreated with ATP for 3 h. The findings indicated that P. gingivalis induced the host defence responses at an early stage. P. gingivalis LPS exerted a more powerful stimulatory effect on the disruption of the epithelial barrier than P. gingivalis. ATP stimulation enhanced the reaction of TJ proteins to P. gingivalis invasion and LPS destruction of the epithelium.

关键词： junctional epithelium periodontitis porphyromonas gingivalis tight junctions

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BET protein inhibitor apabetalone represses porphyromonas gingivalis LPS-induced macrophage M1 polarization via regulating miR-130a/STAT3 axis

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BIOCELL 2022年第10期46卷 2281-2289页

作者： MEIHUA CHEN HUIHUI WANG XIAOFENG CHEN YAN CHEN TIANYING BIAN Department of Periodontics Shanghai Stomatological Hospital&School of StomatologyFudan UniversityShanghai200001China Shanghai Key Laboratory of Craniomaxillofacial Development and Diseases Fudan UniversityShanghai200001China Department of Stomatology Shanghai Fifth People’s HospitalFudan UniversityShanghai200240China

Periodontitis is a frequent chronic inflammatory disorder destroying *** studies have revealed the role of bromodomain and extraterminal domain inhibitor(BETi)and microRNA(miR)-130a in regulating macrophage polarization and pro-inflammatory ***,little is known about whether apabetalone(a novel BETi)and miR-130a are correlated with chronic inflammatory state in periodontitis by regulating macrophage *** murine RAW264.7 macrophages were applied as an in vitro inflammatory *** treatment with porphyromonas gingivalis-derived lipopolysaccharide(Pg LPS)and apabetalone,the expression of macrophage M1 polarization markers and inflammatory cytokines was assessed using real-time PCR,western blot,and enzyme-linked immuno sorbent assay(ELISA).MiR-130a level was assessed using real-time PCR,and the target gene was identified using dual luciferase reporter *** demonstrated that apabetalone repressed Pg LPS-induced macrophage M1 polarization in a dose-dependent manner,as evidenced by decreased expression of inducible nitric oxide synthase(iNOS),CD86,and pro-inflammatory cytokines,and increased expression of Arg-1 and ***,Pg LPS increased miR-130a expression in macrophages,whereas apabetalone treatment repressed the ***,forced expression of miR-130a promoted macrophage M1 polarization,and signal transducer and activator of transcription(STAT)-3 was the direct target gene of miR-130a in the *** together,apabetalone decreases Pg LPS-induced macrophage M1 polarization via regulating miR-130a-3p/STAT3 axis,and may be a promising target for the clinical management of periodontitis.

关键词： Periodontitis Macrophage polarization porphyromonas gingivalis BET inhibitor miRNA

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Association between infection of different strains of porphyromonas gingivalis and Actinobacillus actinomycetemcomitans in subgingival plaque and clinical parameters in chronic periodontitis

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Journal of Zhejiang University-Science B(Biomedicine & Biotechnology) 2007年第2期8卷 121-131页

作者： WU Yan-min YAN Jie CHEN Li-li GU Zhi-yuan Department of Stomatology the Second Affiliated Hospital School of Medicine Zhejiang University Hangzhou 310009 China Department of Medical Microbiology and Parasitology School of Medicine Zhejiang University Hangzhou 310006 China Department of Oral and Maxillofacial Surgery the Affiliated Hospital of Stomatology School of Medicine Zhejiang University Hangzhou 310003 China

Objective： The aim of this study was to investigate subgingival infection frequencies ofporphyromonas gingivalis and Actinobacillus actinomycetemcomitans strains with genetic variation in Chinese chronic periodontitis （CP） patients and to evaluate its correlation with clinical parameters. Methods： Two multiplex polymerase chain reaction （PCR） assays were developed to detect the 16SrDNA, collagenase （prtC） and fimbria （fimA） genes of P. gingivalis and the 16SrDNA, leukotoxin （lktA） and fimbria-associated protein （fap） genes ofA. actinomycetemcomitans in 60 sulcus samples from 30 periodontal healthy subjects and in 122 subgingival plaque samples from 61 patients with CP. The PCR products were further T-A cloned and sent for nucleotide sequence analysis. Results： The 16SrDNA,prtC andfimA genes ofP. gingivalis were detected in 92.6%, 85.2% and 80.3% of the subgingival plaque samples respectively, while the 16SrDNA, lktA andfap genes ofA. actinomycetemcomitans were in 84.4%, 75.4% and 50.0% respectively. Nucleotide sequence analysis showed 98.62%-100% homology of the PCR products in these genes with the reported sequences. P. gingivalis strains with prtC＋/fimA＋ and A. actinomycetemcomitans with lktA＋ were predominant in deep pockets （〉6 mm） or in sites with attachment loss 〉5 mm than in shallow pockets （3-4 mm） or in sites with attachment loss 〈2 mm （P〈0.05）. P. gingivalis strains withprtC＋/fimA＋ also showed higher frequency in gingival index （GI）=3 than in GI=1 group （P〈0.05）. Conclusion： Infection ofP. gingivalis with prtC＋/fimA＋ and A. actinomycetemcomitans with lktA＋ correlates with periodontal destruction of CP in Chinese. Nonetheless P. gingivalis fim4, prtC genes and A. actinomycetem- comitans lktA gene are closely associated with periodontal destruction, while A. actinomycetemcomitansfap gene is not.

关键词： porphyromonas gingivalis Actinobacillus actinomycetemcomitans Strain Periodontitis PCR

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Inhibition and attenuation of pathogenicity of porphyromonas gingivalis by leupeptin： A review

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Frontiers in Biology 2017年第3期12卷 192-198页

作者： Hansa Jain Harsarn Dass Dental College India

BACKGROUND： porphyromonas gingivalis is a periodontal pathogen, which is considered to be a keystone pathogen for periodontitis. A diverse conglomerate of P. gingivalis virulence factors including lipopolysaccharide, fimbriae, capsular polysaccharide, haemagglutinin and cysteine proteases （Arg-gingipains and Lys-gingipain） are considered to be involved in the pathogenesis ofperiodontitis. Leupeptin is a cysteine protease inhibitor which is specific for Arg gingipains. The present review focuses on action of leupeptin on Arg gingipains. METHOD： A search was carried out systematically from the start till September, 2016. The search was made in Medline database via PubMed. The keywords enlisted were ＂leupeptin＂; ＂gingipains＂; ＂periodontitis＂ using Boolean operator ＂and.＂ RESULTS： The result was selection of 58 articles which linked leupeptin to periodontitis and gingipains; pathogenesis of periodontitis, pathogenicity of gingipains and role of leupeptin. CONCLUSION： It was concluded that leupeptin inhibits and attenuates a number of destructive activities of Arg gingipains including inhibition ofplatelet aggregation; inhibit degradation of LL-37, which is an antimicrobial peptide; blocking inhibition ofmonocyte chemoattractant protein; restoring level ofinterleukin-2; inhibiting degradation of collagen type I and IV to name a few.

关键词： porphyromonas gingivalis gingipains leupeptin cysteine protease inhibitor periodontitis

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Suppression of inflammatory gene expression in T cells by porphyromonas gingivalis is mediated by targeting MAPK signaling

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Cellular & Molecular Immunology 2013年第5期10卷 413-422页

作者： Hazem Khalaf Isak Demirel Torbjorn Bengtsson Division of Clinical Medicine School of Health and Medical Sciences Orebro University Orebro Sweden

There is increasing awareness of the effects of porphyromonas gingivalis on host immune responses. Degradation of cytokines and chemokines by cysteine proteinases has previously been reported. However, the precise mechanisms by which P. gingivalis is able to alter intracellular signaling, and thus proliferation and inflammation, have not been descri bed. We have previously reported s u ppression of activator protei n-1 （AP-1） and degradation of I L-2 by protei nases from P. gingivalis. In the present study, we have analyzed the effects of P. gingivalis on Jurkat T-cell signal transduction and subsequent IL-2 and CXCL8 expression. We found that CXCL8, but not IL-2, gene expression levels were significantly suppressed by viable P. gingivalis. Analysis of intracellular signaling revealed an inhibitory effect of P. gingivalis on c-Jun and c-Fos, but not NFκB（p50and p65）, NFATor STAT5expression. This inhibitory effect was not due to suppression of mitogen-activated protein kinase （MAPK）（p38, erkand JNK） gene expression, but was rather due to prevention of protein kinase C （PKC） and p38 phosphorylation, as demonstrated by western blot analysis. Furthermore, SOCS1 and SOCS3 expression levels decreased following treatment of Jurkat T cells with viable P. gingivalis. The results indicate that P. gingivalis is able to suppress inflammatory gene expression by targeting the activity of MAPK pathways in T cells, which was confirmed by using specific inhibitors of NF-κB, PKC, ERK, p38 and JNK.

关键词： MAPK porphyromonas gingivalis protei nases T cells

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Micromolar sodium fluoride mediates anti-osteoclastogenesis in porphyromonas gingivalis-induced alveolar bone loss

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International Journal of Oral Science 2015年第4期7卷 242-249页

作者： Ujjal K Bhawal Hye-Jin Lee Kazumune Arikawa Michiharu Shimosaka Masatoshi Suzuki Toshizo Toyama Takenori Sato Ryota Kawamata Chieko Taguchi Nobushiro Hamada Ikuo Nasu Hirohisa Arakawa Koh Shibutani Department of Biochemistry and Molecular Biology Nihon University School of Dentistry at Matsudo Research Institute of Oral Health Nihon University School of Dentistry at Matsudo Department of Oral Health Graduate School of DentistryKanagawa Dental University Department of Dental Hygiene Howon University Department of Preventive and Public Oral Health Nihon University School of Dentistry at Matsudo Department of Anesthesiology Nihon University School of Dentistry at Matsudo Department of Infection Control Division of MicrobiologyKanagawa Dental University Department of Radiopraxis Science Kanagawa Dental University

Osteoclasts are bone-specific multinucleated cells generated by the differentiation of monocyte/macrophage lineage precursors. Regulation of osteoclast differentiation is considered an effective therapeutic approach to the treatment of bone-lytic diseases. Periodontitis is an inflammatory disease characterized by extensive bone resorption. In this study, we investigated the effects of sodium fluoride （NaF） on osteoclastogenesis induced by porphyromonas gingivalis, an important colonizer of the oral cavity that has been implicated in periodontitis. NaF strongly inhibited the P. gingivalis-induced alveolar bone loss. That effect was accompanied by decreased levels of cathepsin K, interleukin （IL）-1β, matrix metalloproteinase 9 （MMP9）, and tartrate-resistant acid phosphatase, which were up-regulated during P. gingivalis-induced osteoclastogenesis. Consistent with the in vivo anti-osteoclastogenic effect, NaF inhibited osteoclast formation caused by the differentiation factor RANKL （receptor activator of nuclear factor KB ligand） and macrophage colony-stimulating factor （M-CSF）. The RANKL-stimulated induction of the transcription factor nuclear factor of activated T cells （NFAT） cl was also abrogated by NaF. Taken together, our data demonstrate that NaF inhibits RANKL-induced osteoclastogenesis by reducing the induction of NFATcl, ultimately leading to the suppressed expression of cathepsin K and MMP9. The in vivo effect of NaF on the inhibition of P. gingivalis-induced osteoclastogenesis strengthens the potential usefulness of NaF for treating periodontal diseases.

关键词： alveolar bone loss osteoclasts porphyromonas gingivalis sodium fluoride

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Effect of porphyromonas gingivalis PrtC on cytokine expression in ECV304 endothelial cells and its level in subgingival plaques from patients with chronic periodontitis

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Acta Pharmacologica Sinica 2007年第7期28卷 1015-1023页

作者： Yan-min WU~2,Li-li CHEN~(2,6),Jie YAN~(3,6),Chun-yan ZHUANG~4,Zhi-yuan GU~5~2 Department of Stomatology,the Second Affiliated Hospital,College of Medicine,Zhejiang University,Hangzhou 310009,China ~3 Depart-ment of Medical Microbiology and Parasitology,College of Medicine,Zhejiang University,Hangzhou 310006,China ~4 Department ofStomatology,the Affiliated Hospital of the School of Medicine,Ningbo University,Ningbo 315020,China ~5 Department of Oral andMaxillofacial Surgery,the Affiliated Hospital of Stomatology,College of Medicine,Zhejiang University,Hangzhou 310006,China DepartmentofStomatology theSecondAffiliatedHospitalCollegeofMedicineZhejiangUniversityHangzhou310009China DepartmentofMedicalMicrobiologyandParasitology CollegeofMedicineZhejiangUniversityHangzhou310006China

Aim:To investigate the effect of the collagenase gene (prtC) product ofporphyromonas gingivalis on inducing host cells to secrete inflammatorycytokines,and to discuss the correlation between the PrtC level in subgingivalplaque samples and clinical ***:A prokaryotic expression sys-tem pET32a-prtC-Escheria coli BL21 DE3 was *** and im-munoreactivity of the recombinant PrtC protein (rPrtC) was identified by *** was applied to detect interleukin (IL)-1α,IL-8,and TNF-α levelsin supernatants from rPrtC-induced human umbilical vein endothelial cells (HUVEC)originated ECV304 *** parameters recorded at baseline and after treat-ment included bleeding on probing (BOP),probing depth (PD),and attachmentloss (AL).ELISA was established to measure the PrtC level in 196 subgingivalplaque samples from 49 patients with chronic ***:After co-incubation with 1 μg/mL rPrtC for 24 h and with 5 or 10 μg/mL rPrtC for 12 h,thelevels of IL-1α,IL-8,and TNF-α secreted by the ECV304 cells increased signifi-candy (P6 mm PDsites was higher than that in the BOP-negative or the ≤2 mm AL or ≤6 mm PD sites(P6 mm PD sites,the PrtC levels changed insignifi-cantly (P>0.05).Conclusion:rPrtC is able to directly induce host cells to synthe-size and secrete IL-1α,IL-8,and TNF-α.The PrtC level in subgingival samples iscorrelated with BOP,AL,and PD.

关键词： porphyromonas gingivalis collagenase cloning cytokine ELISA

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Intragingival injection of porphyromonas gingivalis-derived lipopolysaccharide induces a transient increase in gingival tumour necrosis factor-a, but not interleukin-6,in anaesthetised rats

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International Journal of Oral Science 2015年第3期7卷 155-160页

作者： Hiroko Taguchi Yuri Aono Takayuki Kawato Masatake Asano Noriyoshi Shimizu Tadashi Saigusa Department of Orthodontics Nihon University School of Dentistry Department of Pharmacology Nihon University School of Dentistry at Matsudo Department of Pharmacology Nihon University School of Dentistry Department of Oral Health Sciences Nihon University School of Dentistry Department of Pathology Nihon University School of Dentistry

This study used in vivo microdialysis to examine the effects of intragingival application of lipopolysaccharide（LPS） derived from porphyromonas gingivalis（Pg-LPS） on gingival tumour necrosis factor（TNF）-a and interleukin（IL）-6 levels in rats. A microdialysis probe with an injection needle attached to the surface of the dialysis membrane was implanted into the gingiva of the upper incisor. For comparison, the effects of LPS derived from Escherichia coli（Ec-LPS） on IL-6 and TNF-a levels were also analysed. Pg-LPS（1 mg/1 m L） or Ec-LPS（1 or 6 mg/1 m L） was applied by microsyringe, with gingival dialysates collected every hour. Enzyme-linked immunosorbent assay（ELISA） revealed that gingival dialysates contained approximately 389 pg？m L21 of IL-6 basally; basal TNF-a levels were lower than the detection limit of the ELISA. Pg-LPS failed to alter IL-6 levels but markedly increased TNF-a levels, which remained elevated for 2 h after treatment. Neither IL-6 nor TNF-a were affected by Ec-LPS. Reverse transcriptase-polymerase chain reaction（RT-PCR） analysis revealed that the gingiva expresses Toll-like receptor（TLR） 2 and TLR4 m RNA. Immunohistochemical examination showed that TLR2 and TLR4 are expressed by gingival epithelial cells. The present study provides in vivo evidence that locally applied Pg-LPS, but not Ec-LPS, into the gingiva transiently increases gingival TNF-a without affecting IL-6. The present results suggest that TLR2 but not TLR4 expressed on gingival epithelial cells may mediate the Pg-LPS-induced increase in gingival TNF-a in rats.

关键词： porphyromonas gingivalis lipopolysaccharide gingiva tumour necrosis factor-a microdialysis

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