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 Metabolic and Community Synergy of Oral Bacteria in Colorectal Cancer

mSphere ◽  
2016 ◽  
Vol 1 (3) ◽  
Author(s):  
Kaitlin J. Flynn ◽  
Nielson T. Baxter ◽  
Patrick D. Schloss
Keyword(s):  
Colorectal Cancer ◽  
Fusobacterium Nucleatum ◽  
Oral Bacteria ◽  
Oral Microbiota ◽  
Community Members ◽  
Content Type ◽  
Bacterial Physiology ◽  
Oral Biofilms ◽  
Two Factors

ABSTRACT The oral periodontopathic bacterium Fusobacterium nucleatum has been repeatedly associated with colorectal tumors. Molecular analysis has identified specific virulence factors that promote tumorigenesis in the colon. However, other oral community members, such as members of the Porphyromonas spp., are also found with F. nucleatum on colonic tumors, and thus, narrow studies of individual pathogens do not take community-wide virulence properties into account. A broader view of oral bacterial physiology and pathogenesis identifies two factors that could promote colonization and persistence of oral bacterial communities in the colon. The polymicrobial nature of oral biofilms and the asaccharolytic metabolism of many of these species make them well suited to life in the microenvironment of colonic lesions. Consideration of these two factors offers a novel perspective on the role of oral microbiota in the initiation, development, and treatment of colorectal cancer.

scholarly journals Protein Tyrosine and Serine/Threonine Phosphorylation in Oral Bacterial Dysbiosis and Bacteria-Host Interaction

2022 ◽  
Vol 11 ◽  
Author(s):  
Liang Ren ◽  
Daonan Shen ◽  
Chengcheng Liu ◽  
Yi Ding
Keyword(s):  
Community Development ◽  
Oral Bacteria ◽  
Bacterial Metabolism ◽  
Oral Microbiota ◽  
Bacterial Protein ◽  
Oral Diseases ◽  
Host Interactions ◽  
Host Interaction ◽  
Systemic Health

The human oral cavity harbors approximately 1,000 microbial species, and dysbiosis of the microflora and imbalanced microbiota-host interactions drive many oral diseases, such as dental caries and periodontal disease. Oral microbiota homeostasis is critical for systemic health. Over the last two decades, bacterial protein phosphorylation systems have been extensively studied, providing mounting evidence of the pivotal role of tyrosine and serine/threonine phosphorylation in oral bacterial dysbiosis and bacteria-host interactions. Ongoing investigations aim to discover novel kinases and phosphatases and to understand the mechanism by which these phosphorylation events regulate the pathogenicity of oral bacteria. Here, we summarize the structures of bacterial tyrosine and serine/threonine kinases and phosphatases and discuss the roles of tyrosine and serine/threonine phosphorylation systems in Porphyromonas gingivalis and Streptococcus mutans, emphasizing their involvement in bacterial metabolism and virulence, community development, and bacteria-host interactions.

scholarly journals Porphyromonas gingivalis Impairs Oral Epithelial Barrier through Targeting GRHL2

2019 ◽  
Vol 98 (10) ◽  
pp. 1150-1158 ◽  
Author(s):  
W. Chen ◽  
A. Alshaikh ◽  
S. Kim ◽  
J. Kim ◽  
C. Chun ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Oral Mucosa ◽  
Porphyromonas Gingivalis ◽  
Oral Bacteria ◽  
Conditional Knockout ◽  
Epithelial Barrier ◽  
Wild Type ◽  
Oral Epithelial ◽  
Junction Proteins

Oral mucosa provides the first line of defense against a diverse array of environmental and microbial irritants by forming the barrier of epithelial cells interconnected by multiprotein tight junctions (TJ), adherens junctions, desmosomes, and gap junction complexes. Grainyhead-like 2 (GRHL2), an epithelial-specific transcription factor, may play a role in the formation of the mucosal epithelial barrier, as it regulates the expression of the junction proteins. The current study investigated the role of GRHL2 in the Porphyromonas gingivalis ( Pg)–induced impairment of epithelial barrier functions. Exposure of human oral keratinocytes (HOK-16B and OKF6 cells) to Pg or Pg-derived lipopolysaccharides ( Pg LPSs) led to rapid loss of endogenous GRHL2 and the junction proteins (e.g., zonula occludens, E-cadherin, claudins, and occludin). GRHL2 directly regulated the expression levels of the junction proteins and the epithelial permeability for small molecules (e.g., dextrans and Pg bacteria). To explore the functional role of GRHL2 in oral mucosal barrier, we used a Grhl2 conditional knockout (KO) mouse model, which allows for epithelial tissue-specific Grhl2 KO in an inducible manner. Grhl2 KO impaired the expression of the junction proteins at the junctional epithelium and increased the alveolar bone loss in the ligature-induced periodontitis model. Fluorescence in situ hybridization revealed increased epithelial penetration of oral bacteria in Grhl2 KO mice compared with the wild-type mice. Also, blood loadings of oral bacteria (e.g., Bacteroides, Bacillus, Firmicutes, β- proteobacteria, and Spirochetes) were significantly elevated in Grhl2 KO mice compared to the wild-type littermates. These data indicate that Pg bacteria may enhance paracellular penetration through oral mucosa in part by targeting the expression of GRHL2 in the oral epithelial cells, which then impairs the epithelial barrier by inhibition of junction protein expression, resulting in increased alveolar tissue destruction and systemic bacteremia.

scholarly journals Central Role of the Early Colonizer Veillonella sp. in Establishing Multispecies Biofilm Communities with Initial, Middle, and Late Colonizers of Enamel

2010 ◽  
Vol 192 (12) ◽  
pp. 2965-2972 ◽  
Author(s):  
Saravanan Periasamy ◽  
Paul E. Kolenbrander
Keyword(s):  
Lactic Acid ◽  
Fluorescent Antibody ◽  
Fusobacterium Nucleatum ◽  
Single Species ◽  
Oral Bacteria ◽  
Flow Cells ◽  
Significant Growth ◽  
Dental Biofilm ◽  
Antibody Staining

ABSTRACT Human dental biofilm communities comprise several species, which can interact cooperatively or competitively. Bacterial interactions influence biofilm formation, metabolic changes, and physiological function of the community. Lactic acid, a common metabolite of oral bacteria, was measured in the flow cell effluent of one-, two- and three-species communities growing on saliva as the sole nutritional source. We investigated single-species and multispecies colonization by using known initial, early, middle, and late colonizers of enamel. Fluorescent-antibody staining and image analysis were used to quantify the biomass in saliva-fed flow cells. Of six species tested, only the initial colonizer Actinomyces oris exhibited significant growth. The initial colonizer Streptococcus oralis produced lactic acid but showed no significant growth. The early colonizer Veillonella sp. utilized lactic acid in two- and three-species biofilm communities. The biovolumes of all two-species biofilms increased when Veillonella sp. was present as one of the partners, indicating that this early colonizer promotes mutualistic community development. All three-species combinations exhibited enhanced growth except one, i.e., A. oris, Veillonella sp., and the middle colonizer Porphyromonas gingivalis, indicating specificity among three-species communities. Further specificity was seen when Fusobacterium nucleatum (a middle colonizer), Aggregatibacter actinomycetemcomitans (a late colonizer), and P. gingivalis did not grow with S. oralis in two-species biofilms, but inclusion of Veillonella sp. resulted in growth of all three-species combinations. We propose that commensal veillonellae use lactic acid for growth in saliva and that they communicate metabolically with initial, early, middle, and late colonizers to establish multispecies communities on enamel.

scholarly journals TGF-β1 Inhibits TLR-mediated Odontoblast Responses to Oral Bacteria

2009 ◽  
Vol 88 (4) ◽  
pp. 333-338 ◽  
Author(s):  
O.V. Horst ◽  
K.A. Tompkins ◽  
S.R. Coats ◽  
P.H. Braham ◽  
R.P. Darveau ◽  
...  
Keyword(s):  
Cell Surface ◽  
Tissue Repair ◽  
Lactobacillus Casei ◽  
Tooth Development ◽  
Fusobacterium Nucleatum ◽  
Poor Response ◽  
Oral Bacteria ◽  
Cellular Processes ◽  
Tgf Β1

TGF-β1 exerts diverse functions in tooth development and tissue repair, but its role in microbial defenses of the tooth is not well-understood. Odontoblasts extending their cellular processes into the dentin are the first cells to recognize signals from TGF-β1 and bacteria in carious dentin. This study aimed to determine the role of TGF-β1 in modulating odontoblast responses to oral bacteria. We show that these responses depend upon the expression levels of microbial recognition receptors TLR2 and TLR4 on the cell surface. Porphyromonas gingivalis, Prevotella intermedia, and Fusobacterium nucleatum activated both TLRs, but TLR4 played a greater role. Lack of cell-surface TLR2 was associated with poor response to Streptococcus mutans, Enterococcus faecalis, and Lactobacillus casei. TGF-β1 inhibited TLR2 and TLR4 expression and attenuated odontoblast responses. Our findings suggest that the balance between TLR-mediated inflammation and TGF-β1 anti-inflammatory activity plays an important role in pulpal inflammation.

scholarly journals Role of Fusobacterium nucleatum and Coaggregation in Anaerobe Survival in Planktonic and Biofilm Oral Microbial Communities during Aeration

1998 ◽  
Vol 66 (10) ◽  
pp. 4729-4732 ◽  
Author(s):  
David J. Bradshaw ◽  
Philip D. Marsh ◽  
G. Keith Watson ◽  
Clive Allison
Keyword(s):  
Anaerobic Bacteria ◽  
Fusobacterium Nucleatum ◽  
Oral Bacteria ◽  
Obligate Anaerobe ◽  
Obligately Anaerobic ◽  
Prevotella Nigrescens ◽  
Tolerant Species ◽  
Species Pairs ◽  
Planktonic Phase

ABSTRACT Coaggregation is a well-characterized phenomenon by which specific pairs of oral bacteria interact physically. The aim of this study was to examine the patterns of coaggregation between obligately anaerobic and oxygen-tolerant species that coexist in a model oral microbial community. Obligate anaerobes other than Fusobacterium nucleatum coaggregated only poorly with oxygen-tolerant species. In contrast, F. nucleatum was able to coaggregate not only with both oxygen-tolerant and other obligately anaerobic species but also with otherwise-noncoaggregating obligate anaerobe–oxygen-tolerant species pairs. The effects of the presence or absence of F. nucleatum on anaerobe survival in both the biofilm and planktonic phases of a complex community of oral bacteria grown in an aerated (gas phase, 200 ml of 5% CO2 in air · min−1) chemostat system were then investigated. In the presence of F. nucleatum, anaerobes persisted in high numbers (>107 · ml−1 in the planktonic phase and >107 · cm−2 in 4-day biofilms). In an equivalent culture in the absence of F. nucleatum, the numbers of black-pigmented anaerobes (Porphyromonas gingivalis and Prevotella nigrescens) were significantly reduced (P ≤ 0.001) in both the planktonic phase and in 4-day biofilms, while the numbers of facultatively anaerobic bacteria increased in these communities. Coaggregation-mediated interactions between F. nucleatum and other species facilitated the survival of obligate anaerobes in aerated environments.

scholarly journals miR-188-5p Suppresses Gastric Cancer Cell Proliferation and Invasion via Targeting ZFP91

2018 ◽  
Vol 27 (1) ◽  
pp. 65-71 ◽  
Author(s):  
Yuping Peng ◽  
Xuning Shen ◽  
Honggang Jiang ◽  
Zhiheng Chen ◽  
Jiaming Wu ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Cell Proliferation ◽  
Inverse Correlation ◽  
Migration And Invasion ◽  
Normal Tissues ◽  
Promising Therapeutic Target ◽  
Cellular Apoptosis ◽  
Gastric Cancer Cell Proliferation

MicroRNAs (miRNAs) have been demonstrated to be essential regulators in the development and progression of various cancers. The role of miR-188-5p in gastric cancer (GC) has not been determined. In this study, we found that the expression of miR-188-5p was downregulated in GC tissues compared with adjacent normal tissues. The lowly expressed miR-188-5p was significantly associated with lymph node metastasis and advanced TNM stage. Moreover, overexpression of miR-188-5p significantly inhibited GC cell proliferation, migration, and invasion but promoted cellular apoptosis. Mechanistically, we identified transcription factor ZFP91 as a target gene of miR-188-5p in GC. We found that miR-188-5p overexpression significantly inhibited the expression of ZFP91 in GC cell lines. There was an inverse correlation between the expression of miR-188-5p and ZFP91 in GC tissues. We found that restoration of ZFP91 in miR-188-5p-overexpressed MGC-803 and SGC-7901 cells promoted cell proliferation, migration, and invasion. Finally, we also showed that overexpression of miR-188-5p inhibited tumor growth in vivo. Taken together, our findings indicated that miR-188-5p serves as a tumor suppressor in human GC by targeting ZFP91, suggesting that miR-188-5p might be a promising therapeutic target for GC treatment.

Streptococcus salivarius Promotes Mucin Putrefaction and Malodor Production by Porphyromonas gingivalis

2006 ◽  
Vol 85 (10) ◽  
pp. 910-914 ◽  
Author(s):  
N. Sterer ◽  
M. Rosenberg
Keyword(s):  
Porphyromonas Gingivalis ◽  
Potential Role ◽  
Oral Microbiota ◽  
Streptococcus Salivarius ◽  
Oral Malodor ◽  
Gram Positive ◽  
Gram Negative ◽  
Sds Page ◽  
Micro Organisms

Although the contribution of the oral microbiota to oral malodor is well-documented, the potential role of Gram-positive micro-organisms is unclear. In the current study, we tested the hypothesis that Gram-positive micro-organisms contribute to malodor production by deglycosylating oral glycoproteins, rendering them susceptible to subsequent proteolysis. To this end, we examined the effect of Streptococcus salivarius on Porphyromonas gingivalis-mediated putrefaction of a model glycoprotein (pig gastric mucin). Malodor was scored by two odor judges, and volatile sulfides were determined with the use of a sulfide monitor. Mucin degradation was followed by electrophoresis on SDS-PAGE. Results showed that the addition of S. salivarius or β-galactosidase promoted mucin degradation and concomitant malodor production. Addition of glycosidic inhibitors (p-APTG and glucose) inhibited this process. These results suggest that Gram-positive micro-organisms such as S. salivarius contribute to oral malodor production by deglycosylating salivary glycoproteins, thus exposing their protein core to further degradation by Gram-negative micro-organisms.

scholarly journals SAT0590 ORAL MICROBIOTA IDENTIFIES PATIENTS WITH EARLY RHEUMATOID ARTHRITIS

2020 ◽  
Vol 79 (Suppl 1) ◽  
pp. 1254.2-1254
Author(s):  
A. Esberg ◽  
L. Johansson ◽  
I. Johansson ◽  
S. Rantapää Dahlqvist
Keyword(s):  
Rheumatoid Arthritis ◽  
Porphyromonas Gingivalis ◽  
Aggregatibacter Actinomycetemcomitans ◽  
Oral Bacteria ◽  
Diagnostic Tools ◽  
Oral Microbiota ◽  
Healthy Controls ◽  
Periodontal Pathogens ◽  
Specificity And Sensitivity ◽  
Periodontal Infection

Background:Several studies have suggested a link between the two chronic inflammatory diseases, rheumatoid arthritis (RA) and periodontitis (PD) [1]. The diseases share similar environmental and genetic risks factors,e.g.,smoking [2] and the HLA-DRB1 alleles [3]. Several serum markers used in the diagnosis of RA have also been found to be elevated in PD,e.g.,anti-citrullinated proteins antibodies (ACPA) and rheumatoid factor (RF) [4]. The connection between PD and RA has been suggested to be explained by several periodontal pathogens,e.g., Aggregatibacter actinomycetemcomitansandPorphyromonas gingivalis, which have been suggested to induce the production of autoantibodies [5, 6].Objectives:To investigate the composition of the concerted saliva microbiota and its role in the development of RA, with the aim of improving the diagnostic tools.Methods:16S ribosomal RNA gene sequencing of saliva bacterial DNA isolated from a total of 61 early RA (eRA) patients and 59 healthy controls was made. The eRA (symptoms ≤ 12 months) was diagnosed at an Early Arthritis Clinic (fulfilling the 1987 ARA criteria) and matched with the controls for sex and age, except for two of the elderly cases. None of the individuals included in the study had taken antibiotics during the preceding 3 months. No one of the cases were treated with anti-rheumatic drugs except for corticosteroids in 16 cases the latest month.Results:All participants were classified into three hierarchical cluster groups based on their saliva microbiota and the distribution of eRA cases versus controls differed distinctly between the cluster groups. The microbiota from the eRA had higher species richness, differed in beta-diversity, and was enriched for species in the Fusobacterium and Porphyromonas genera, and for the Alloprevotella tannerae, Campylobacter gracilis, Capnocytophaga leadbetteri, Filifactor alocis, Fusobacterium nucleatum subsp. polymorphum, Neisseria elongate, Porphyromionas endodontalis and Prevotella pleuritidis species compared to controls. Combining two topped ranked species,A. tanneraeandCatonella morbisignificantly predicted eRA with an AUC score of 0.86 and a specificity and sensitivity of 0.80 and 0.85, respectively.The predicted functions of the microbiota in eRA patients were dominated by fatty acid metabolism, ornithine metabolism, glucosylceramidase, sphingolipids, beta-lactamase resistance, biphenyl degradation and 17-beta-estradiol 17-dehydrogenase metabolism.Conclusion:In this study a difference in oral microbiota diversity between eRA patients and healthy controls could be shown. Some of the eRA-associated oral bacteria have previously been suggested to play an aetiological role in the development of RA, but others have not been recognized earlier, such as A. tannerae, F. alocis, F. nucleatum subsp. polymorphum, and P. endodontalis, and may therefore be useful in RA risk assessment.References:[1]Fuggle, N.R., et al.,Hand to Mouth: A Systematic Review and Meta-Analysis of the Association between Rheumatoid Arthritis and Periodontitis.Front Immunol, 2016. 7: p. 80.[2]Heliovaara, M., et al.,Smoking and risk of rheumatoid arthritis.J Rheumatol, 1993. 20(11): p. 1830-5.[3]Katz, J., et al.,Human leukocyte antigen (HLA) DR4. Positive association with rapidly progressing periodontitis.J Periodontol, 1987. 58(9): p. 607-10.[4]Mikuls, T.R., et al.,Periodontitis and Porphyromonas gingivalis in patients with rheumatoid arthritis.Arthritis Rheumatol, 2014. 66(5): p. 1090-100.[5]Konig, M.F., et al.,Aggregatibacter actinomycetemcomitans-induced hypercitrullination links periodontal infection to autoimmunity in rheumatoid arthritis.Sci Transl Med, 2016. 8(369): p. 369ra176.[6]Rosenstein, E.D., et al.,Hypothesis: the humoral immune response to oral bacteria provides a stimulus for the development of rheumatoid arthritis.Inflammation, 2004. 28(6): p. 311-8.Disclosure of Interests:None declared

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