| Fusobacterium nucleatum | |
|---|---|
Scientific classification | |
| Domain: | Bacteria |
| Kingdom: | Fusobacteriati |
| Phylum: | Fusobacteriota |
| Class: | Fusobacteriia |
| Order: | Fusobacteriales |
| Family: | Fusobacteriaceae |
| Genus: | Fusobacterium |
| Species: | F. nucleatum |
| Binomial name | |
| Fusobacterium nucleatum Knorr, 1922 | |
Fusobacterium nucleatum is aGram-negative,anaerobicbacterium,commensal to the humanoral cavity, that plays a role inperiodontal disease. This organism is commonly recovered from different monocultured microbial and mixed infections in humans and animals. In health and disease, it is a key component of periodontalplaque due to its abundance and its ability to coaggregate with other bacteria species in the oral cavity.[1][2]
Research implicates periodontal disease caused byF. nucleatum withpreterm births in humans. In many studies,F. nucleatum cells have been isolated from theamniotic fluid,placenta, andchorioamnionic membranes of womendelivering prematurely. Moreover, laboratory mice intravenously inoculated withF. nucleatum have been found to deliver prematurely, and the pathology of the infection seems to mirror observations in humans.[3] Together, this research provides evidence for a possible causal connection betweenF. nucleatum-caused periodontal disease and at least some cases of preterm delivery.F. nucleatum can also be isolated from thevaginal microbiome, especially in women with a condition known asbacterial vaginosis.[4] BothF. nucleatum vaginal colonization and bacterial vaginosis also have been linked with preterm birth and infections within the uterus.[5] Thus, preterm birth arising by infections caused byF. nucleatum could also arise from invasive infection into the uterine tissue originating from the colonized vagina.[citation needed]
F. nucleatum has a demonstrated association withcolorectal cancer.Fusobacterium species have been found at higher quantities in certain types of colon tumors than in surrounding colon tissue or the colons of healthy individuals, but whether this is an indirect correlation or a causal link is unclear. A distinguishing mechanism has been described by whichF. nucleatum creates a pro-inflammatory environment which is conducive totumor growth through the recruitment oftumor-infiltrating immune cells, which, unlike other bacteria linked to colorectal carcinoma, does not exacerbate other pathological processes such ascolitis,enteritis and inflammatory-associated intestinal carcinogenesis. This suggests direct and specific carcinogenesis.[6]F. nucleatum can bind to host tissueE-cadherins via a FadA, an outer membrane protein.[7] Additionally, a surface expressedlectin called Fap2 mediatesF. nucleatum adherence to colorectal cancer cells that expressGal/GalNAc moieties on their surface. Binding via Fap2 has also been shown to up-regulate production ofcytokines associated with higher rates ofmetastasis.[8]
Type IV pili facilitatenatural competence inF. nucleatum.[9] Natural competence involves three principal stages: (1) Uptake of exogenousDNA and transport to the cytoplasm, (2) homologous DNA that has been taken up can integrate into the recipient cell genome byhomologous recombination, and (3) the integrated exogenous DNA can expressgene functions.[9]
{{cite journal}}:Cite journal requires|journal= (help)