Mobile Microbiome: Oral Bacteria in Extra-oral Infections and Inflammation
Yiping W. Han,X. Wang +1 more
TLDR
The most recent findings on systemic infections and inflammation complicated by oral bacteria, including cardiovascular disease, adverse pregnancy outcomes, rheumatoid arthritis, inflammatory bowel disease and colorectal cancer, respiratory tract infections, and organ inflammations and abscesses are reviewed.Abstract:
The link between oral infections and adverse systemic conditions has attracted much attention in the research community. Several mechanisms have been proposed, including spread of the oral infection due to transient bacteremia resulting in bacterial colonization in extra-oral sites, systemic injury by free toxins of oral pathogens, and systemic inflammation caused by soluble antigens of oral pathogens. Mounting evidence supports a major role of the systemic spread of oral commensals and pathogens to distant body sites causing extra-oral infections and inflammation. We review here the most recent findings on systemic infections and inflammation complicated by oral bacteria, including cardiovascular disease, adverse pregnancy outcomes, rheumatoid arthritis, inflammatory bowel disease and colorectal cancer, respiratory tract infections, and organ inflammations and abscesses. The recently identified virulence mechanisms of oral species Fusobacterium nucleatum, Porphyromonas gingivalis, Streptococcus mutans, and Campylobacter rectus are also reviewed. A pattern emerges indicating that only select subtype(s) of a given species, e.g., F. nucleatum subspecies animalis and polymorphum and S. mutans non-c serotypes, are prone to extra-oral translocation. These findings advocate the importance of identification and quantification of potential pathogens at the subtype levels for accurate prediction of disease potential.read more
Citations
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The Placenta Harbors a Unique Microbiome
TL;DR: A unique placental microbiome niche was characterized, composed of nonpathogenic commensal microbiota from the Firmicutes, Tenericute, Proteobacteria, Bacteroidetes, and Fusobacteria phyla, which was consistently different from those reported in other parts of the body, including the skin and urogenital tract.
Journal ArticleDOI
Periodontitis: from microbial immune subversion to systemic inflammation
TL;DR: The mechanisms of microbial immune subversion that tip the balance from homeostasis to disease in oral or extra-oral sites are discussed.
Journal ArticleDOI
The oral microbiota: dynamic communities and host interactions.
TL;DR: Current knowledge and emerging mechanisms governing oral polymicrobial synergy and dysbiosis that have both enhanced the understanding of pathogenic mechanisms and aided the design of innovative therapeutic approaches for oral diseases are discussed.
Journal ArticleDOI
Binding of the Fap2 protein of Fusobacterium nucleatum to human inhibitory receptor TIGIT protects tumors from immune cell attack.
Chamutal Gur,Yara Ibrahim,Batya Isaacson,Rachel Yamin,Jawad Abed,Moriya Gamliel,Jonatan Enk,Yotam Bar-On,Noah Stanietsky-Kaynan,Shunit Coppenhagen-Glazer,Noam Shussman,Gideon Almogy,Angelica Cuapio,Erhard Hofer,Dror Mevorach,Adi Tabib,Rona Ortenberg,Gal Markel,Karmela Miklić,Stipan Jonjić,Caitlin A. Brennan,Wendy S. Garrett,Gilad Bachrach,Ofer Mandelboim +23 more
TL;DR: This work has shown that natural killer cell killing of various tumors is inhibited in the presence of various F. nucleatum strains, and identified a bacterium-dependent, tumor-immune evasion mechanism in which tumors exploit the Fap2 protein of F. nucleus to inhibit immune cell activity via TIGIT.
Journal ArticleDOI
Immunomicrobial pathogenesis of periodontitis: keystones, pathobionts, and host response.
TL;DR: New paradigms in the understanding of periodontitis are discussed, which may shed light into other polymicrobial inflammatory disorders and highlight gaps in knowledge required for an integrated picture of the interplay between microbes and innate and adaptive immune elements that initiate and propagate chronic periodontal inflammation.
References
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Fusobacterium nucleatum infection is prevalent in human colorectal carcinoma
Mauro Castellarin,René L. Warren,J. Douglas Freeman,Lisa Dreolini,Martin Krzywinski,Jaclyn Strauss,Rebecca O Barnes,Peter H. Watson,Emma Allen-Vercoe,Richard A. Moore,Robert A. Holt +10 more
TL;DR: Overabundance of Fusobacterium sequences in tumor versus matched normal control tissue is verified by quantitative PCR analysis from a total of 99 subjects, and a positive association with lymph node metastasis is observed.
Journal ArticleDOI
Genomic analysis identifies association of Fusobacterium with colorectal carcinoma
Aleksandar Kostic,Dirk Gevers,Chandra Sekhar Pedamallu,Chandra Sekhar Pedamallu,Monia Michaud,Fujiko Duke,Fujiko Duke,Ashlee M. Earl,Akinyemi I. Ojesina,Akinyemi I. Ojesina,Joonil Jung,Adam J. Bass,Adam J. Bass,Josep Tabernero,José Baselga,Chen Liu,Ramesh A. Shivdasani,Shuji Ogino,Bruce W. Birren,Curtis Huttenhower,Curtis Huttenhower,Wendy S. Garrett,Wendy S. Garrett,Matthew Meyerson,Matthew Meyerson +24 more
TL;DR: The composition of the microbiota in colorectal carcinoma is characterized using whole genome sequences from nine tumor/normal pairs and Fusobacterium sequences were enriched in carcinomas, confirmed by quantitative PCR and 16S rDNA sequence analysis of 95 carcinoma/normal DNA pairs.
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Identification of periodontal pathogens in atheromatous plaques.
TL;DR: periodontal pathogens are present in atherosclerotic plaques where, like other infectious microorganisms such as C. pneumoniae, they may play a role in the development and progression of atherosclerosis leading to coronary vascular disease and other clinical sequelae.
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Low-Abundance Biofilm Species Orchestrates Inflammatory Periodontal Disease through the Commensal Microbiota and Complement
George Hajishengallis,Shuang Liang,Mark A. Payne,Ahmed Hashim,Ravi Jotwani,Mehmet A. Eskan,Megan L. McIntosh,Asil Alsam,Keith L. Kirkwood,John D. Lambris,Richard P. Darveau,Michael A. Curtis +11 more
TL;DR: It is shown that P. gingivalis, at very low colonization levels, triggers changes to the amount and composition of the oral commensal microbiota leading to inflammatory periodontal bone loss, demonstrating that a single, low-abundance species can disrupt host-microbial homeostasis to cause inflammatory disease.