scholarly journals The efficacy of sarang semut extract (Myrmecodia pendens Merr & Perry) in inhibiting Porphyromonas gingivalis biofilm formation

2017 ◽  
Vol 50 (2) ◽  
pp. 55
Author(s):  
Zulfan M. Alibasyah ◽  
Ambrosius Purba ◽  
Budi Setiabudiawan ◽  
Hendra Dian Adhita ◽  
Dikdik Kurnia ◽  
...  
Keyword(s):  
Oral Cavity ◽  
Porphyromonas Gingivalis ◽  
Biofilm Formation ◽  
Pathogenic Bacteria ◽  
Positive Control ◽  
Host Cells ◽  
Control Treatment ◽  
Natural Material ◽  
Violet Crystal ◽  
Mass Profile

Background: Porphyromonas gingivalis (P. gingivalis) is a pathogenic bacteria present in the oral cavity involved in the pathogenesis of chronic periodontitis and biofilm. This mass of microorganisms represents one of the virulent factors of P. gingivalis which plays an important role as an attachment initiator in host cells. Sarang semut is a natural material possessing the ability to inhibit the growth of P. gingivalis. Purpose: This study aims to analyze the effect of sarang semut extract on the formation of P. gingivalis biofilm. Methods: The study used methanol sarang semut extract and P. gingivalis ATCC 33277 and phosphomycin as a positive control. Treatment was initiated by means of culturing. Biofilm test and P. gingivalis biofilm formation observation were subsequently performed by means of a light microscope at a magnification of 400x. Results: The formation of P. gingivalis biofilms tended to increase at 3, 6, and 9 hours. Results of the violet crystal test showed that concentrations of 100% and 75% of the sarang semut extract successfully inhibited the formation of P. gingivalis biofilm according to the incubation time. Meanwhile, the sarang semut extracts at concentrations of 50%, 25%, 12.5%, and 6.125% resulted in weak inhibition of the formation of P. gingivalis biofilm. The biofilm mass profile observed by a microscope tended to decrease as an indicator of the effects of the sarang semut extract. Conclusion: Sarang semut extract can inhibit the formation of P. gingivalis biofilm, especially at concentrations of 100% and 75%. Nevertheless, phosphomycin has stronger antibiofilm of P. gingivalis effects than those of the sarang semut extract at all of the concentrations listed above.

scholarly journals Effect of Lonicera caerulea var. emphyllocalyx Fruit on Biofilm Formed by Porphyromonas gingivalis

2019 ◽  
Vol 2019 ◽  
pp. 1-9 ◽  
Author(s):  
Masaaki Minami ◽  
Hiroshi Takase ◽  
Mineo Nakamura ◽  
Toshiaki Makino
Keyword(s):  
Oral Cavity ◽  
Porphyromonas Gingivalis ◽  
Aspiration Pneumonia ◽  
Biofilm Formation ◽  
Bacterial Colonization ◽  
Bacterial Biofilm ◽  
Dependent Manner ◽  
Electron Microscopic ◽  
Concentration Dependent Manner ◽  
Lonicera Caerulea

Porphyromonas gingivalis is an important pathogenic anaerobic bacterium that causes aspiration pneumonia. This bacterium frequently forms biofilms in the oral cavity and in respiratory tract-associated medical devices. Bacterial colonization that occurs in association with this biofilm formation is the main reason for incurable aspiration pneumonia. The Lonicera caerulea var. emphyllocalyx (LCE) fruit has been used in folk medicine in Hokkaido, the northern part of Japan. The aim of this study was to elucidate one of the antimicrobial mechanisms of LCE methanol extract (LCEE)—the inhibitory effect of LCEE on biofilm formation by P. gingivalis. Our results show that LCEE significantly reduced biofilm formation by three different P. gingivalis isolates in a concentration- and time-dependent manner that were quantified by the adsorption of safranin red. When LCEE was added to biofilms already formed by P. gingivalis, LCEE did not degrade the biofilm. However, treatment with LCEE significantly promoted the removal of existing biofilm by vibration compared to that of control. We also confirmed biofilm formation in LCEE-treated P. gingivalis in tracheal tubes using scanning electron microscopic (SEM) analysis. Cyanidin 3-O-glucoside (C3G), one of the components of LCE, also inhibited the formation of biofilm by P. gingivalis in a concentration-dependent manner. Our results reveal that LCEE may be an effective antibacterial substance for P. gingivalis-induced aspiration pneumonia because of its role in the suppression of bacterial biofilm formation in the oral cavity.

scholarly journals Porphyromonas gingivalis galE Is Involved in Lipopolysaccharide O-Antigen Synthesis and Biofilm Formation

2006 ◽  
Vol 74 (11) ◽  
pp. 6145-6153 ◽  
Author(s):  
Ryoma Nakao ◽  
Hidenobu Senpuku ◽  
Haruo Watanabe
Keyword(s):  
Oral Cavity ◽  
Periodontal Disease ◽  
Porphyromonas Gingivalis ◽  
Parental Strain ◽  
Biofilm Formation ◽  
Gene Knockout ◽  
Partial Recovery ◽  
Wild Type ◽  
O Antigen ◽  
Crucial Component

ABSTRACT Porphyromonas gingivalis is a crucial component of complex plaque biofilms that form in the oral cavity, resulting in the progression of periodontal disease. To elucidate the mechanism of periodontal biofilm formation, we analyzed the involvement of several genes related to the synthesis of polysaccharides in P. gingivalis. Gene knockout P. gingivalis mutants were constructed by insertion of an ermF-ermAM cassette; among these mutants, the galE mutant showed some characteristic phenotypes involved in the loss of GalE activity. As expected, the galE mutant accumulated intracellular carbohydrates in the presence of 0.1% galactose and did not grow in the presence of galactose at a concentration greater than 1%, in contrast to the parental strain. Lipopolysaccharide (LPS) analysis indicated that the length of the O-antigen chain of the galE mutant was shorter than that of the wild type. It was also demonstrated that biofilms generated by the galE mutant had an intensity 4.5-fold greater than those of the wild type. Further, the galE mutant was found to be significantly susceptible to some antibiotics in comparison with the wild type. In addition, complementation of the galE mutation led to a partial recovery of the parental phenotypes. We concluded that the galE gene plays a pivotal role in the modification of LPS O antigen and biofilm formation in P. gingivalis and considered that our findings of a relationship between the function of the P. gingivalis galE gene and virulence phenotypes such as biofilm formation may provide clues for understanding the mechanism of pathogenicity in periodontal disease.

Porphyromonas gingivalis-Epithelial Cell Interactions in Periodontitis

2006 ◽  
Vol 85 (5) ◽  
pp. 392-403 ◽  
Author(s):  
E. Andrian ◽  
D. Grenier ◽  
M. Rouabhia
Keyword(s):  
Epithelial Cells ◽  
Periodontal Disease ◽  
Porphyromonas Gingivalis ◽  
Pathogenic Bacteria ◽  
Current Knowledge ◽  
Oral Bacteria ◽  
Host Cells ◽  
Host Responses ◽  
Tissue Destruction ◽  
Adaptive Ability

Emerging data on the consequences of the interactions between invasive oral bacteria and host cells have provided new insights into the pathogenesis of periodontal disease. Indeed, modulation of the mucosal epithelial barrier by pathogenic bacteria appears to be a critical step in the initiation and progression of periodontal disease. Periodontopathogens such as Porphyromonas gingivalis have developed different strategies to perturb the structural and functional integrity of the gingival epithelium. P. gingivalis adheres to, invades, and replicates within human epithelial cells. Adhesion of P. gingivalis to host cells is multimodal and involves the interaction of bacterial cell-surface adhesins with receptors expressed on the surfaces of epithelial cells. Internalization of P. gingivalis within host cells is rapid and requires both bacterial contact-dependent components and host-induced signaling pathways. P. gingivalis also subverts host responses to bacterial challenges by inactivating immune cells and molecules and by activating host processes leading to tissue destruction. The adaptive ability of these pathogens that allows them to survive within host cells and degrade periodontal tissue constituents may contribute to the initiation and progression of periodontitis. In this paper, we review current knowledge on the molecular cross-talk between P. gingivalis and gingival epithelial cells in the development of periodontitis.

Extracellular galectin-1 enhances adhesion to and invasion of oral epithelial cells by Porphyromonas gingivalis

2018 ◽  
Vol 64 (7) ◽  
pp. 465-471 ◽  
Author(s):  
Riyoko Tamai ◽  
Michiyo Kobayashi-Sakamoto ◽  
Yusuke Kiyoura
Keyword(s):  
Porphyromonas Gingivalis ◽  
Pathogenic Bacteria ◽  
Host Cells ◽  
Epithelial Cell Line ◽  
Lectin Receptors ◽  
Gram Negative ◽  
Oral Epithelial Cells ◽  
Gingival Epithelial Cell ◽  
Galectin 3 ◽  
Adhesion And Invasion

Galectin-1 and galectin-3 are C-type lectin receptors that bind to lipopolysaccharide in the cell wall of gram-negative bacteria. In this study, we investigated the effects of galectin-1 and galectin-3 on adhesion to and invasion of the human gingival epithelial cell line Ca9-22 by Porphyromonas gingivalis, a periodontal pathogenic gram-negative bacterium. Recombinant galectin-1, but not galectin-3, enhanced P. gingivalis adhesion and invasion, although both galectins bound similarly to P. gingivalis. Flow cytometry also revealed that Ca9-22 cells express low levels of galectin-1 and moderate levels of galectin-3. Ca9-22 cells in which galectin-3 was knocked-down did not exhibit enhanced P. gingivalis adhesion and invasion. Similarly, specific antibodies to galectin-1 and galectin-3 did not inhibit P. gingivalis adhesion and invasion. These results suggest that soluble galectin-1, but not galectin-3, may exacerbate periodontal disease by enhancing the adhesion to and invasion of host cells by periodontal pathogenic bacteria.

scholarly journals Comparison of Biofilm and Attachment Mechanisms of a Phytopathological and Clinical Isolate ofKlebsiella pneumoniaeSubsp.pneumoniae

2013 ◽  
Vol 2013 ◽  
pp. 1-6 ◽  
Author(s):  
Adriana Marcia Nicolau Korres ◽  
Gloria Maria de Farias V. Aquije ◽  
David S. Buss ◽  
Jose Aires Ventura ◽  
Patricia Machado Bueno Fernandes ◽  
...  
Keyword(s):  
Clinical Isolate ◽  
Biofilm Formation ◽  
Pathogenic Bacteria ◽  
Bacterial Species ◽  
High Vacuum ◽  
Positive Control ◽  
Stress Factors ◽  
Atomic Force ◽  
Human Food Chain ◽  
Pineapple Fruit

Some bacterial species can colonize humans and plants. It is almost impossible to prevent the contact of clinically pathogenic bacteria with food crops, and if they can persist there, they can reenter the human food chain and cause disease. On the leaf surface, microorganisms are exposed to a number of stress factors. It is unclear how they survive in such different environments. By increasing adhesion to diverse substrates, minimizing environmental differences, and providing protection against defence mechanisms, biofilms could provide part of the answer.Klebsiella pneumoniaesubsp.pneumoniaeis clinically important and also associated with fruit diseases, such as “pineapple fruit collapse.” We aimed to characterize biofilm formation and adhesion mechanisms of this species isolated from pineapple in comparison with a clinical isolate. No differences were found between the two isolates quantitatively or qualitatively. Both tested positive for capsule formation and were hydrophobic, but neither produced adherence fibres, which might account for their relatively weak adhesion compared to the positive controlStaphylococcus epidermidisATCC 35984. Both produced biofilms on glass and polystyrene, more consistently at 40°C than 35°C, confirmed by atomic force and high-vacuum scanning electron microscopy. Biofilm formation was maintained in an acidic environment, which may be relevant phytopathologically.

scholarly journals Edwardsiella piscicida YefM-YoeB: A Type II Toxin-Antitoxin System That Is Related to Antibiotic Resistance, Biofilm Formation, Serum Survival, and Host Infection

2021 ◽  
Vol 12 ◽  
Author(s):  
Dongmei Ma ◽  
Hanjie Gu ◽  
Yanjie Shi ◽  
Huiqin Huang ◽  
Dongmei Sun ◽  
...  
Keyword(s):  
Biofilm Formation ◽  
Pathogenic Bacteria ◽  
Wild Strain ◽  
Host Cells ◽  
Resistant Bacteria ◽  
Serum Resistance ◽  
Type Ii ◽  
Edwardsiella Piscicida

The emergence of drug resistant bacteria is a tricky and confronted problem in modern medicine, and one of important reasons is the widespread of toxin-antitoxin (TA) systems in pathogenic bacteria. Edwardsiella piscicida (also known as E. tarda) is the leading pathogen threatening worldwide fresh and seawater aquaculture industries and has been considered as a model organism for studying intracellular and systemic infections. However, the role of type II TA systems are completely unknown in aquatic pathogenic bacteria. In this study, we identified and characterized a type II TA system, YefM-YoeB, of E. piscicida, where YefM is the antitoxin and YoeB is the toxin. yefM and yoeB are co-expressed in a bicistronic operon. When expressed in E. coli, YoeB cause bacterial growth arrest, which was restored by the addition of YefM. To investigate the biological role of the TA system, two markerless yoeB and yefM-yoeB in-frame mutant strains, TX01ΔyoeB and TX01ΔyefM-yoeB, were constructed, respectively. Compared to the wild strain TX01, TX01ΔyefM-yoeB exhibited markedly reduced resistance against oxidative stress and antibiotic, and markedly reduced ability to form persistent bacteria. The deletion of yefM-yoeB enhanced the bacterial ability of high temperature tolerance, biofilm formation, and host serum resistance, which is the first study about the relationship between type II TA system and serum resistance. In vitro infection experiment showed that the inactivation of yefM-yoeB greatly enhanced bacterial capability of adhesion in host cells. Consistently, in vivo experiment suggested that the yefM-yoeB mutation had an obvious positive effect on bacteria dissemination of fish tissues and general virulence. Introduction of a trans-expressed yefM-yoeB restored the virulence of TX01ΔyefM-yoeB. These findings suggest that YefM-YoeB is involved in responding adverse circumstance and pathogenicity of E. piscicida. In addition, we found that YefM-YoeB negatively autoregulated the expression of yefM-yoeB and YefM could directly bind with own promoter. This study provides first insights into the biological activity of type II TA system YefM-YoeB in aquatic pathogenic bacteria and contributes to understand the pathogenesis of E. piscicida.

scholarly journals Role of the Clp System in Stress Tolerance, Biofilm Formation, and Intracellular Invasion in Porphyromonas gingivalis

2007 ◽  
Vol 190 (4) ◽  
pp. 1436-1446 ◽  
Author(s):  
Cindy A. Capestany ◽  
Gena D. Tribble ◽  
Kazuhiko Maeda ◽  
Donald R. Demuth ◽  
Richard J. Lamont
Keyword(s):  
Epithelial Cells ◽  
Porphyromonas Gingivalis ◽  
Biofilm Formation ◽  
Pathogenic Bacteria ◽  
Opportunistic Pathogen ◽  
Protein Subunit ◽  
Gingival Epithelial Cells ◽  
Clp Proteases ◽  
Stress Response System ◽  
Intracellular Invasion

ABSTRACT Clp proteases and chaperones are ubiquitous among prokaryotes and eukaryotes, and in many pathogenic bacteria the Clp stress response system is also involved in regulation of virulence properties. In this study, the roles of ClpB, ClpC, and ClpXP in stress resistance, homotypic and heterotypic biofilm formation, and intracellular invasion in the oral opportunistic pathogen Porphyromonas gingivalis were investigated. Absence of ClpC and ClpXP, but not ClpB, resulted in diminished tolerance to high temperatures. Response to oxidative stress was not affected by the loss of any of the Clp proteins. The clpC and clpXP mutants demonstrated elevated monospecies biofilm formation, and the absence of ClpXP also enhanced heterotypic P. gingivalis-Streptococcus gordonii biofilm formation. All clp mutants adhered to gingival epithelial cells to the same level as the wild type; however, ClpC and ClpXP were found to be necessary for entry into host epithelial cells. ClpB did not play a role in entry but was required for intracellular replication and survival. ClpXP negatively regulated the surface exposure of the minor fimbrial (Mfa) protein subunit of P. gingivalis, which stimulates biofilm formation but interferes with epithelial cell entry. Collectively, these results show that the Clp protease complex and chaperones control several processes that are important for the colonization and survival of P. gingivalis in the oral cavity.

scholarly journals Association of Mitogen-Activated Protein Kinase Pathways with Gingival Epithelial Cell Responses to Porphyromonas gingivalis Infection

2001 ◽  
Vol 69 (11) ◽  
pp. 6731-6737 ◽  
Author(s):  
Kiyoko Watanabe ◽  
Özlem Yilmaz ◽  
Simin F. Nakhjiri ◽  
Carol M. Belton ◽  
Richard J. Lamont
Keyword(s):  
Protein Kinase ◽  
Map Kinase ◽  
Porphyromonas Gingivalis ◽  
Pathogenic Bacteria ◽  
Specific Inhibitor ◽  
Host Cells ◽  
Periodontal Pathogen ◽  
Dependent Manner ◽  
Mitogen Activated Protein ◽  
Map Kinase Pathways

ABSTRACT Mitogen-activated protein (MAP) kinase pathways are key factors in host signaling events and can also play important roles in the internalization of pathogenic bacteria by host cells.Porphyromonas gingivalis, a periodontal pathogen, can efficiently invade human gingival epithelial cells (GECs). In this study, we examined the activation of MAP kinase pathways in GECs infected with P. gingivalis. c-Jun N-terminal kinase (JNK) was activated after 5 min of infection with P. gingivalis, whereas noninvasiveStreptococcus gordonii did not have a significant effect on JNK activation. In contrast, extracellular signal-regulated kinase (ERK) 1/2 was downregulated in a dose-dependent manner by P. gingivalis, but not by S. gordonii, after a 15-min exposure. Nonmetabolically active P. gingivaliscells were unable to modulate MAP kinase activity. U0126, a specific inhibitor of MEK1/2 (ERK1/2 kinase), and toxin B, a specific inhibitor of Rho family GTPases, had no effect on P. gingivalis invasion. Genistein, a tyrosine protein kinase inhibitor, blocked uptake of P. gingivalis. The transcriptional regulator NF-κB was not activated by P. gingivalis. These results suggest that P. gingivalis can selectively target components of the MAP kinase pathways. ERK1/2, while not involved in P. gingivalisinvasion of GECs, may be downregulated by internalized P. gingivalis. Activation of JNK is associated with the invasive process of P. gingivalis.

scholarly journals Preliminary study on the inhibitory effect of seaweed Gracilaria verrucosa extract on biofilm formation of Candida albicans cultured from the saliva of a smoker

F1000Research ◽  
2018 ◽  
Vol 7 ◽  
pp. 684
Author(s):  
Zaki Mubarak ◽  
Adintya Humaira ◽  
Basri A. Gani ◽  
Zainal A. Muchlisin
Keyword(s):  
Candida Albicans ◽  
Immune System ◽  
Antifungal Activity ◽  
Oral Cavity ◽  
Virulence Factors ◽  
Biofilm Formation ◽  
Inhibitory Effect ◽  
Positive Control ◽  
Multiple Factors ◽  
Preliminary Study

Background: Candida albicans is an opportunistic fungus that infects the oral cavity. Increases in colony numbers of C. albicans can be caused by multiple factors, such as smoking, a weakened immune system, taking antibiotics and with immune-compromised individuals. Smoking can increase the virulence factor of C. albicans and make it stronger. One of the virulence factors of C. albicans is the biofilm it forms. The C. albicans biofilm makes it more tolerant to extracts of the seaweed Gracilaria verrucosa, which has antifungal activity. The objective of the study was to examine the ability of the G. verrucosa extracts to inhibit the formation of biofilm by C. albicans obtained from the saliva of smoker. Methods: A total of six concentrations of G. verrucosa (6.25, 12.5, 25, 50, 75 and 100%) were tested in this study. The positive control was fluconazole 0.31 µg/ml C. albicans was taken from the saliva of one smoker in Faculty of Dentistry, Syiah Kuala University. The total amount of biofilm was assessed using an ELISA reader. The data were subjected to Kruskal-Wallis test at a significance limit of p<0.05. Results: The seaweed extract has three bio-active compounds: steroids, terpenoid, and tannins. The results showed that the inhibitory activity of seaweed on C. albicans biofilm formation increases as its concentration increases. The highest effectiveness was recorded at a seaweed concentration of 100% at 48 h of exposure. Conclusions: The optimal inhibition of the C. albicans biofilm formation was recorded at the concentration of 100% G. verrucosa after 48 hours of exposure.

scholarly journals Structural Characterization of Peptide-Mediated Inhibition of Porphyromonas gingivalis Biofilm Formation

2006 ◽  
Vol 74 (10) ◽  
pp. 5756-5762 ◽  
Author(s):  
Carlo Amorin Daep ◽  
DeAnna M. James ◽  
Richard J. Lamont ◽  
Donald R. Demuth
Keyword(s):  
Amino Acids ◽  
Oral Cavity ◽  
Porphyromonas Gingivalis ◽  
Biofilm Formation ◽  
Hydrophobic Interactions ◽  
Specific Activity ◽  
Combinatorial Libraries ◽  
Structural Features ◽  
Periodontal Pathogen ◽  
Active Site Residues

ABSTRACT Porphyromonas gingivalis is a periodontal pathogen whose primary niche is the anaerobic environment of subgingival dental plaque, but initial colonization of the oral cavity is likely to occur on supragingival surfaces that already support robust biofilm communities. Our studies have shown that P. gingivalis adheres to Streptococcus gordonii through interaction of the minor fimbrial antigen Mfa1 with a specific region of the streptococcal SspB polypeptide (residues 1167 to 1193) designated BAR. We show that a synthetic peptide comprising the BAR sequence potently inhibits P. gingivalis adherence to S. gordonii (50% inhibitory concentration = 1.3 μM) and prevents the development of P. gingivalis biofilms. However, a retroinverso peptide that possessed the same side chain topology as that of BAR was inactive, suggesting that interactions of Mfa1 with the peptide backbone of BAR are important for binding. A conformationally constrained analog of BAR inhibited P. gingivalis adherence and biofilm formation but at a lower specific activity than that of BAR. Therefore, to further define the structural features of the Mfa1-BAR interaction, we functionally screened combinatorial libraries of BAR in which active site residues (Asn1182, Thr1184, and Val1185) were replaced with each of the 19 common amino acids. Peptides containing positively charged amino acids at position 1182 or hydrophobic residues at position 1185 bound P. gingivalis more efficiently than did control peptides containing Asn and Val at these positions, suggesting that electrostatic and hydrophobic interactions may contribute to Mfa1-SspB binding. In contrast, replacement of Pro or Gly at these positions was detrimental to adherence, suggesting that perturbation of the BAR secondary structure influences activity. The net effect of substitutions for Thr1184 was less pronounced either positively or negatively than that at the other sites. These results define physicochemical characteristics of the interacting interface of Mfa1 and SspB and suggest that peptides or peptidomimetics with greater specific inhibitory activity than that of BAR can be developed. These compounds may represent potential therapeutics that target some of the first molecular interactions that allow P. gingivalis to colonize the oral cavity.

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