Fusobacterium nucleatum
| Fusobacterium nucleatum | |
|---|---|
Scientific classification 
| |
| Domain: | Bacteria |
| Phylum: | Fusobacteriota |
| Class: | Fusobacteriia |
| Order: | Fusobacteriales |
| Family: | Fusobacteriaceae |
| Genus: | Fusobacterium |
| Species: | F. nucleatum |
| Binomial name | |
| Fusobacterium nucleatum Knorr, 1922 | |
Fusobacterium nucleatum is a Gram-negative, anaerobic bacterium, commensal to the human oral cavity, that plays a role in periodontal 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 periodontal plaque due to its abundance and its ability to coaggregate with other bacteria species in the oral cavity.[1][2]
Preterm births
Research implicates periodontal disease caused by F. nucleatum with preterm births in humans. In many studies, F. nucleatum cells have been isolated from the amniotic fluid, placenta, and chorioamnionic membranes of women delivering prematurely. Moreover, laboratory mice intravenously inoculated with F. 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 between F. nucleatum-caused periodontal disease and at least some cases of preterm delivery. F. nucleatum can also be isolated from the vaginal microbiome, especially in women with a condition known as bacterial vaginosis.[4] Both F. 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 by F. nucleatum could also arise from invasive infection into the uterine tissue originating from the colonized vagina.[citation needed]
Colon cancer
F. nucleatum has a demonstrated association with colorectal 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 which F. nucleatum creates a pro-inflammatory environment which is conducive to tumor growth through the recruitment of tumor-infiltrating immune cells, which, unlike other bacteria linked to colorectal carcinoma, does not exacerbate other pathological processes such as colitis, enteritis and inflammatory-associated intestinal carcinogenesis. This suggests direct and specific carcinogenesis.[6] F. nucleatum can bind to host tissue E-cadherins via a FadA, an outer membrane protein.[7] Additionally, a surface expressed lectin called Fap2 mediates F. nucleatum adherence to colorectal cancer cells that express Gal/GalNAc moieties on their surface. Binding via Fap2 has also been shown to up-regulate production of cytokines associated with higher rates of metastasis.[8]
Natural competence
Type IV pili facilitate natural competence in F. nucleatum.[9] Natural competence involves three principal stages: (1) Uptake of exogenous DNA and transport to the cytoplasm, (2) homologous DNA that has been taken up can integrate into the recipient cell genome by homologous recombination, and (3) the integrated exogenous DNA can express gene functions.[9]
See also
References
- ^ Kapatral V, Anderson I, Ivanova N, Reznik G, Los T, Lykidis A, et al. (April 2002). "Genome sequence and analysis of the oral bacterium Fusobacterium nucleatum strain ATCC 25586". Journal of Bacteriology. 184 (7): 2005–18. doi:10.1128/JB.184.7.2005-2018.2002. PMC 134920. PMID 11889109.
- ^ "Fusobacterium nucleatumin Periodontal Health and Disease". Current Issues in Molecular Biology. 2011. doi:10.21775/cimb.013.025.
- ^ Han YW, Redline RW, Li M, Yin L, Hill GB, McCormick TS (April 2004). "Fusobacterium nucleatum induces premature and term stillbirths in pregnant mice: implication of oral bacteria in preterm birth". Infection and Immunity. 72 (4): 2272–9. doi:10.1128/IAI.72.4.2272-2279.2004. PMC 375172. PMID 15039352.
- ^ Hillier SL, Krohn MA, Rabe LK, Klebanoff SJ, Eschenbach DA (June 1993). "The normal vaginal flora, H2O2-producing lactobacilli, and bacterial vaginosis in pregnant women". Clinical Infectious Diseases. 16 (Suppl 4): S273-81. doi:10.1093/clinids/16.supplement_4.s273. PMID 8324131.
- ^ Hitti J, Hillier SL, Agnew KJ, Krohn MA, Reisner DP, Eschenbach DA (February 2001). "Vaginal indicators of amniotic fluid infection in preterm labor". Obstetrics and Gynecology. 97 (2): 211–9. doi:10.1016/s0029-7844(00)01146-7. PMID 11165584. S2CID 345396.
- ^ Kostic AD, Chun E, Robertson L, Glickman JN, Gallini CA, Michaud M, et al. (August 2013). "Fusobacterium nucleatum potentiates intestinal tumorigenesis and modulates the tumor-immune microenvironment". Cell Host & Microbe. 14 (2): 207–15. doi:10.1016/j.chom.2013.07.007. PMC 3772512. PMID 23954159.
- ^ Guo, Pin; Tian, Zibin; Kong, Xinjuan; Yang, Lin; Shan, Xinzhi; Dong, Bingzi; Ding, Xueli; Jing, Xue; Jiang, Chen; Jiang, Na; Yu, Yanan (2020-09-29). "FadA promotes DNA damage and progression of Fusobacterium nucleatum-induced colorectal cancer through up-regulation of chk2". Journal of Experimental & Clinical Cancer Research. 39 (1): 202. doi:10.1186/s13046-020-01677-w. ISSN 1756-9966. PMC 7523382. PMID 32993749.
- ^ Casasanta, Michael A.; Yoo, Christopher C.; Udayasuryan, Barath; Sanders, Blake E.; Umaña, Ariana; Zhang, Yao; Peng, Huaiyao; Duncan, Alison J.; Wang, Yueying (2020-01-16). "Fusobacterium nucleatum host cell binding and invasion induces IL-8 and CXCL1 secretion that drives colorectal cancer cell migration". doi:10.1101/2020.01.15.907931. S2CID 213030137. Retrieved 2022-07-18.
{{cite journal}}: Cite journal requires|journal=(help) - ^ a b Sanders BE, Umaña A, Nguyen TTD, Williams KJ, Yoo CC, Casasanta MA, Wozniak B, Slade DJ. Type IV pili facilitated natural competence in Fusobacterium nucleatum. Anaerobe. 2023 Aug;82:102760. doi: 10.1016/j.anaerobe.2023.102760. Epub 2023 Jul 13. PMID: 37451427