scholarly journals Protein interactions between the oral bacteria Fusobacterium nucleatum and Porphyromonas gingivalis in biofilm and planktonic culture

2020 ◽  
Author(s):  
Marwan Mansoor Ali Mohammed ◽  
Veronika Kuchařová Pettersen ◽  
Audun H. Nerland ◽  
Harald G. Wiker ◽  
Vidar Bakken
Keyword(s):  
Porphyromonas Gingivalis ◽  
Protein Interactions ◽  
Fusobacterium Nucleatum ◽  
Oral Bacteria ◽  
Cell Contact ◽  
P Value ◽  
Bacterial Cells ◽  
Label Free ◽  
Planktonic Culture ◽  
Oral Biofilm

AbstractThe opportunistic pathogens Fusobacterium nucleatum and Porphyromonas gingivalis are Gram-negative bacteria associated with oral biofilm and periodontal disease. Although liquid cultures are often the preferred cultivation method in microbiology, bacterial cells in biofilm adopt a profoundly different phenotype reflecting the close cell-to-cell contact compare to their planktonic counterparts. To investigate F. nucleatum and P. gingivalis interactions relevant in biofilm formation, we applied liquid chromatography-tandem mass spectrometry to determine the expressed proteome of F. nucleatum and P. gingivalis cells that were grown either as biofilm or in planktonic culture, and individually or together.The proteomic analyses detected 1,322 F. nucleatum and 966 P. gingivalis proteins. We statistically compared the proteins label-free quantitative (LFQ) intensities between biofilm and planktonic culture and identified significant changes (p-value ≤0.05) in 0,4% F. nucleatum proteins, 7% P. gingivalis proteins, and more than 14% of all proteins in the dual-species model. For both species, proteins involved in vitamin B2 (riboflavin) metabolic process had significantly increased levels in the biofilm condition. In both mono- and dual-species biofilm models, P. gingivalis increased the production of proteins functional in translation, oxidation-reduction, and amino acid metabolism, when compared to planktonic cultures. However, when we compared LFQ intensities between mono- and dual-species models, over 90% of the significantly changed P. gingivalis proteins had their levels reduced in biofilm and planktonic settings of the dual-species model.Our findings suggest that the two bacteria interact with each other at the protein level and indicate that P. gingivalis reduces the production of multiple proteins because of more favourable growth conditions provided by F. nucleatum presence. The results highlight the complex interactions of bacteria contributing to oral biofilm, which need to be considered in the design of future prevention strategies.

scholarly journals HIV-1 Reactivation Induced by the Periodontal Pathogens Fusobacterium nucleatum and Porphyromonas gingivalis Involves Toll-Like Receptor 4 and 9 Activation in Monocytes/Macrophages

2010 ◽  
Vol 17 (9) ◽  
pp. 1417-1427 ◽  
Author(s):  
Octavio A. González ◽  
Mengtao Li ◽  
Jeffrey L. Ebersole ◽  
Chifu B. Huang
Keyword(s):  
Porphyromonas Gingivalis ◽  
Inflammatory Diseases ◽  
Fusobacterium Nucleatum ◽  
Oral Bacteria ◽  
Viral Reactivation ◽  
Toll Like Receptor ◽  
Periodontal Pathogens ◽  
Necrosis Factor Alpha ◽  
Tlr9 Activation ◽  
Hiv 1

ABSTRACT Although oral coinfections (e.g., periodontal disease) are highly prevalent in human immunodeficiency virus type 1-positive (HIV-1+) patients and appear to positively correlate with viral load levels, the potential for oral bacteria to induce HIV-1 reactivation in latently infected cells has received little attention. We showed that HIV-1 long terminal repeat (LTR) promoter activation can be induced by periodontopathogens in monocytes/macrophages; nevertheless, the mechanisms involved in this response remain undetermined. Since Toll-like receptor 2 (TLR2), TLR4, and TLR9 activation have been involved in HIV-1 recrudescence, we sought to determine the role of these TLRs in HIV-1 reactivation induced by the periodontal pathogens Fusobacterium nucleatum and Porphyromonas gingivalis using BF24 monocytes/macrophages stably transfected with the HIV-1 promoter driving chloramphenicol acetyltransferase (CAT) expression and THP89GFP cells, a model of HIV-1 latency. We demonstrated that TLR9 activation by F. nucleatum and TLR2 activation by both bacteria appear to be involved in HIV-1 reactivation; however, TLR4 activation had no effect. Moreover, the autocrine activity of tumor necrosis factor alpha (TNF-α) but not interleukin-1β (IL-1β) produced in response to bacteria could impact viral reactivation. The transcription factors NF-κB and Sp1 appear to be positively regulating HIV-1 reactivation induced by these oral pathogens. These results suggest that oral Gram-negative bacteria (F. nucleatum and P. gingivalis) associated with oral and systemic chronic inflammatory disorders enhance HIV-1 reactivation in monocytes/macrophages through TLR2 and TLR9 activation in a mechanism that appears to be transcriptionally regulated. Increased bacterial growth and emergence of these bacteria or their products accompanying chronic oral inflammatory diseases could be risk modifiers for viral replication, systemic immune activation, and AIDS progression in HIV-1+ patients.

scholarly journals Role of Oral Microbiota in Cancer Development

2019 ◽  
Vol 7 (1) ◽  
pp. 20 ◽  
Author(s):  
Tomasz Karpiński
Keyword(s):  
Cell Proliferation ◽  
Porphyromonas Gingivalis ◽  
Fusobacterium Nucleatum ◽  
Oral Bacteria ◽  
Cancer Development ◽  
Oral Microbiota ◽  
Cellular Apoptosis ◽  
Bacterial Stimulation ◽  
Specific Species

Nowadays cancer is the second main cause of death in the world. The most known bacterial carcinogen is Helicobacter pylori. Pathogens that can have an impact on cancer development in the gastrointestinal tract are also found in the oral cavity. Some specific species have been identified that correlate strongly with oral cancer, such as Streptococcus sp., Peptostreptococcus sp., Prevotella sp., Fusobacterium sp., Porphyromonas gingivalis, and Capnocytophaga gingivalis. Many works have also shown that the oral periopathogens Fusobacterium nucleatum and Porphyromonas gingivalis play an important role in the development of colorectal and pancreatic cancer. Three mechanisms of action have been suggested in regard to the role of oral microbiota in the pathogenesis of cancer. The first is bacterial stimulation of chronic inflammation. Inflammatory mediators produced in this process cause or facilitate cell proliferation, mutagenesis, oncogene activation, and angiogenesis. The second mechanism attributed to bacteria that may influence the pathogenesis of cancers by affecting cell proliferation is the activation of NF-κB and inhibition of cellular apoptosis. In the third mechanism, bacteria produce some substances that act in a carcinogenic manner. This review presents potentially oncogenic oral bacteria and possible mechanisms of their action on the carcinogenesis of human cells.

scholarly journals Matrix-Bound Zolzoledronate Enhances the Biofilm Colonization of Hydroxyapatite: Effects on Osteonecrosis

Antibiotics ◽  
2021 ◽  
Vol 10 (11) ◽  
pp. 1380
Author(s):  
Ranya Elsayed ◽  
Ahmed El-Awady ◽  
Christopher Cutler ◽  
Zoya Kurago ◽  
Mahmoud Elashiry ◽  
...  
Keyword(s):  
Alveolar Bone ◽  
Fusobacterium Nucleatum ◽  
Osteonecrosis Of The Jaw ◽  
Oral Bacteria ◽  
Defect Model ◽  
Oral Biofilm ◽  
Bacterial Proliferation ◽  
Dental Procedures ◽  
Matrix Bound

(1) Background: The aim of this study was to test whether matrix-bound zoledronate (zol) molecules enhanced the oral biofilm colonization of a mineralized matrix, rendering the alveolar bone more susceptible to medication-related osteonecrosis of the jaw (MRONJ) following invasive dental procedures. (2) Methods: We tested the effect of matrix-bound zol on the growth and attachment of Porphyromonas gingivalis (Pg), Fusobacterium nucleatum (Fn) and Actinomyces israelii (Ai), and whether the nitrogen-containing component of zol contributed to such effect. The role of oral bacteria in the induction of osteonecrosis was then tested using an extra-oral bone defect model. (3) Results: The attachment of biofilm to hydroxyapatite discs increased when the discs were pre-treated with zol. Bacterial proliferation was not affected. Matrix-bound zol was more potent than non-nitrogen-containing etidronate in enhancing the colonization. Stimulation was dampened by pre-treating the bacteria with histidine. The delivery of oral biofilm to a tibial defect caused osteonecrosis in zol-treated rats. (4) Conclusions: We conclude that matrix-bound zol enhances the oral biofilm colonization of hydroxyapatite. This enhancement depended on the presence of the nitrogen-containing group. The oral biofilm rendered the extra-oral bone susceptible to medication-related osteonecrosis, suggesting that it has an important role in the induction of MRONJ.

Attachment of oral bacteria to titanium surfaces: An SEM study

1994 ◽  
Vol 52 ◽  
pp. 468-469
Author(s):  
J. E. Laffoon ◽  
R. L. Anderson ◽  
J. C. Keller ◽  
C. D. Wu-Yuan
Keyword(s):  
Technical Problem ◽  
Titanium Implant ◽  
Oral Bacteria ◽  
Bacterial Cells ◽  
Thin Sections ◽  
Surface Ultrastructure ◽  
Sem Study ◽  
Key Factor ◽  
Titanium Surfaces

Titanium (Ti) dental implants have been used widely for many years. Long term implant failures are related, in part, to the development of peri-implantitis frequently associated with bacteria. Bacterial adherence and colonization have been considered a key factor in the pathogenesis of many biomaterial based infections. Without the initial attachment of oral bacteria to Ti-implant surfaces, subsequent polymicrobial accumulation and colonization leading to peri-implant disease cannot occur. The overall goal of this study is to examine the implant-oral bacterial interfaces and gain a greater understanding of their attachment characteristics and mechanisms. Since the detailed cell surface ultrastructure involved in attachment is only discernible at the electron microscopy level, the study is complicated by the technical problem of obtaining titanium implant and attached bacterial cells in the same ultra-thin sections. In this study, a technique was developed to facilitate the study of Ti implant-bacteria interface.Discs of polymerized Spurr’s resin (12 mm x 5 mm) were formed to a thickness of approximately 3 mm using an EM block holder (Fig. 1). Titanium was then deposited by vacuum deposition to a film thickness of 300Å (Fig. 2).

Label-Free Mass Spectrometry-Based Plasma Proteomics Identified LY6D, DSC3, CDSN, SERPINB12, and SLURP1,as Novel Protein Biomarkers For Pulmonary Tuberculosis

2019 ◽  
Vol 17 ◽  
Author(s):  
Xiaoli Yu ◽  
Lu Zhang ◽  
Na Li ◽  
Peng Hu ◽  
Zhaoqin Zhu ◽  
...  
Keyword(s):  
Pulmonary Tuberculosis ◽  
Search Algorithm ◽  
Differentially Expressed ◽  
P Value ◽  
Plasma Samples ◽  
Label Free ◽  
Protein Biomarkers ◽  
Protein Database ◽  
Leave One Out ◽  
Potential Biomarkers

Aim: We aimed to identify new plasma biomarkers for the diagnosis of Pulmonary tuberculosis. Background: Tuberculosis is an ancient infectious disease that remains one of the major global health problems. Until now, effective, convenient, and affordable methods for diagnosis of Pulmonary tuberculosis were still lacked. Objective: This study focused on construct a label-free LC-MS/MS based comparative proteomics between six tuberculosis patients and six healthy controls to identify differentially expressed proteins (DEPs) in plasma. Method: To reduce the influences of high-abundant proteins, albumin and globulin were removed from plasma samples using affinity gels. Then DEPs from the plasma samples were identified using a label-free Quadrupole-Orbitrap LC-MS/MS system. The results were analyzed by the protein database search algorithm SEQUEST-HT to identify mass spectra to peptides. The predictive abilities of combinations of host markers were investigated by general discriminant analysis (GDA), with leave-one-out cross-validation. Results: A total of 572 proteins were identified and 549 proteins were quantified. The threshold for differentially expressed protein was set as adjusted p-value < 0.05 and fold change ≥1.5 or ≤0.6667, 32 DEPs were found. ClusterVis, TBtools, and STRING were used to find new potential biomarkers of PTB. Six proteins, LY6D, DSC3, CDSN, FABP5, SERPINB12, and SLURP1, which performed well in the LOOCV method validation, were termed as potential biomarkers. The percentage of cross-validated grouped cases correctly classified and original grouped cases correctly classified is greater than or equal to 91.7%. Conclusion: We successfully identified five candidate biomarkers for immunodiagnosis of PTB in plasma, LY6D, DSC3, CDSN, SERPINB12, and SLURP1. Our work supported this group of proteins as potential biomarkers for pulmonary tuberculosis, and be worthy of further validation.

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