The role of coaggregation between Porphyromonas gingivalis and Fusobacterium nucleatum on the host response to mixed infection

2012 ◽  
Vol 39 (7) ◽  
pp. 617-625 ◽  
Author(s):  
David Polak ◽  
Lior Shapira ◽  
Ervin I. Weiss ◽  
Yael Houri-Haddad
Keyword(s):  
Porphyromonas Gingivalis ◽  
Mixed Infection ◽  
Host Response ◽  
Fusobacterium Nucleatum

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.

Prior exposure of mice to Fusobacterium nucleatum modulates host response to Porphyromonas gingivalis

2001 ◽  
Vol 16 (6) ◽  
pp. 338-344 ◽  
Author(s):  
J. Choi ◽  
M. A. Borrello ◽  
E. Smith ◽  
C. W. Cutler ◽  
H. Sojar ◽  
...  
Keyword(s):  
Porphyromonas Gingivalis ◽  
Host Response ◽  
Fusobacterium Nucleatum ◽  
Prior Exposure

scholarly journals Systems Biology and Bile Acid Signalling in Microbiome-Host Interactions in the Cystic Fibrosis Lung

Antibiotics ◽  
2021 ◽  
Vol 10 (7) ◽  
pp. 766
Author(s):  
David F. Woods ◽  
Stephanie Flynn ◽  
Jose A. Caparrós-Martín ◽  
Stephen M. Stick ◽  
F. Jerry Reen ◽  
...  
Keyword(s):  
Cystic Fibrosis ◽  
Bile Acids ◽  
Host Response ◽  
Signal Molecules ◽  
Therapeutic Approaches ◽  
Related Factors ◽  
Host Interactions ◽  
Important Host ◽  
Respiratory Microbiota

The study of the respiratory microbiota has revealed that the lungs of healthy and diseased individuals harbour distinct microbial communities. Imbalances in these communities can contribute to the pathogenesis of lung disease. How these imbalances occur and establish is largely unknown. This review is focused on the genetically inherited condition of Cystic Fibrosis (CF). Understanding the microbial and host-related factors that govern the establishment of chronic CF lung inflammation and pathogen colonisation is essential. Specifically, dissecting the interplay in the inflammation–pathogen–host axis. Bile acids are important host derived and microbially modified signal molecules that have been detected in CF lungs. These bile acids are associated with inflammation and restructuring of the lung microbiota linked to chronicity. This community remodelling involves a switch in the lung microbiota from a high biodiversity/low pathogen state to a low biodiversity/pathogen-dominated state. Bile acids are particularly associated with the dominance of Proteobacterial pathogens. The ability of bile acids to impact directly on both the lung microbiota and the host response offers a unifying principle underpinning the pathogenesis of CF. The modulating role of bile acids in lung microbiota dysbiosis and inflammation could offer new potential targets for designing innovative therapeutic approaches for respiratory disease.

scholarly journals Lipopolysaccharides of Fusobacterium nucleatum and Porphyromonas gingivalis increase RANKL-expressing neutrophils in air pouches of mice

2021 ◽  
Vol 37 (1) ◽  
Author(s):  
Ae Ri Kim ◽  
Yun Kyong Lim ◽  
Joong-Ki Kook ◽  
Eun-Jung Bak ◽  
Yun-Jung Yoo
Keyword(s):  
Flow Cytometry ◽  
Porphyromonas Gingivalis ◽  
Osteoclast Differentiation ◽  
Fusobacterium Nucleatum ◽  
Pathological Changes ◽  
Air Pouch ◽  
E Coli ◽  
Differentiation Factor ◽  
Osteoclast Differentiation Factor

AbstractIncreases of neutrophils and osteoclasts are pathological changes of periodontitis. RANKL is an osteoclast differentiation factor. The effect of periodontopathogen LPS on RANKL-expressing neutrophils has not been clarified yet. We evaluated numerical changes of RANKL-expressing neutrophils in air pouches of mice injected with LPSs of Fusobacterium nucleatum and Porphyromonas gingivalis. Mice with air pouches were assigned into saline (C)-, E. coli LPS- (Ec LPS)-, F. nucleatum LPS (Fn LPS)-, P. gingivalis LPS (Pg LPS)-, and Fn LPS and Pg LPS (Fn + Pg LPS)-injected groups. CD11b+Ly6G+ neutrophils and CD11b+Ly6G+RANKL+ neutrophils in blood and air pouch exudates were determined by flow cytometry. In blood, compared to the C group, the Fn LPS group showed increases of CD11b+Ly6G+ neutrophils and CD11b+Ly6G+RANKL+ neutrophils whereas the Pg LPS group showed no significant differences. These increases in the Fn LPS group were not different to those in the Ec LPS group. In exudates, Fn LPS and Pg LPS groups showed increases of CD11b+Ly6G+ neutrophils and CD11b+Ly6G+RANKL+ neutrophils compared to the C group. Increased levels in the Fn LPS group were not different to those in the Ec LPS group, but Pg LPS group was lower than those in the Ec LPS group. In blood and exudates, the Fn + Pg LPS group showed no difference in levels of these neutrophils compared to the Ec LPS group. LPSs of F. nucleatum and P. gingivalis increased RANKL-expressing neutrophils although the degrees of increases were different. These suggest that periodontopathogen LPS can act as a stimulant to increase RANKL-expressing neutrophils.

scholarly journals Bacteriocin-like activity of oral Fusobacterium nucleatum isolated from human and non-human primates

1999 ◽  
Vol 30 (4) ◽  
pp. 324-346 ◽  
Author(s):  
Elerson Gaetti-Jardim Júnior ◽  
Mario Julio Avila-Campos
Keyword(s):  
Oral Cavity ◽  
Microbial Ecology ◽  
Dental Plaque ◽  
Fusobacterium Nucleatum ◽  
Antagonistic Activity ◽  
Healthy Individuals ◽  
Bacterial Microbiota ◽  
Reference Strains

Fusobacterium nucleatum is indigenous of the human oral cavity and has been involved in different infectious processes. The production of bacteriocin-like substances may be important in regulation of bacterial microbiota in oral cavity. The ability to produce bacteriocin-like substances by 80 oral F. nucleatum isolates obtained from periodontal patients, healthy individuals and Cebus apella monkeys, was examinated. 17.5% of all tested isolates showed auto-antagonism and 78.8% iso- or hetero-antagonism. No isolate from monkey was capable to produce auto-inhibition. In this study, the antagonistic substances production was variable in all tested isolates. Most of the F. nucleatum showed antagonistic activity against tested reference strains. These data suggest a possible participation of these substances on the oral microbial ecology in humans and animals. However, the role of bacteriocins in regulating dental plaque microbiota in vivo is discussed.

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