The DOI matches its Crossref record; 9 of the 9 references it cites were found in a registry or an index.
The inflammophilic character of the periodontitis‐associated microbiota
Open accessAbstract
Summary: In periodontitis, dysbiotic microbial communities exhibit synergistic interactions for enhanced protection from host defenses, nutrient acquisition, and persistence in an inflammatory environment. This review discusses evidence that periodontitis‐associated communities are ‘inflammo‐philic’ (=loving or attracted to inflammation) in that they have evolved to not only endure inflammation but also to take advantage of it. In this regard, inflammation can drive the selection and enrichment of these pathogenic communities by providing a source of nutrients in the form of tissue breakdown products (e.g. degraded collagen peptides and heme‐containing compounds). In contrast, those species that cannot benefit from the altered ecological conditions of the inflammatory environment, or for which host inflammation is detrimental, are likely to be outcompeted. Consistent with the concept that inflammation fosters the growth of dysbiotic microbial communities, the bacterial biomass of human periodontitis‐associated biofilms was shown to increase with increasing periodontal inflammation. Conversely, anti‐inflammatory treatments in animal models of periodontitis were shown to diminish the periodontal bacterial load, in addition to protecting from bone loss. The selective flourishing of inflammophilic bacteria can perpetuate inflammatory tissue destruction by setting off a ‘vicious cycle’ for disease progression, in which dysbiosis and inflammation reinforce each other. Therefore, the control of inflammation appears to be central to the treatment of periodontitis, as it is likely to control both dysbiosis and disease progression.
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Cites
Complement: a key system for immune surveillance and homeostasis
Ricklin, D., Hajishengallis, G., Yang, K., & Lambris, J. D. (2010) · Nature Immunology · doi:10.1038/ni.1923 · Cited by 3,654 · cited 1×
“…activation of complement, P. gingivalis retains its capacity to colonize the periodontium of C3-deficient ( C3 –/– ) mice (Maekawa et al ., 2014a), in which complement cannot be activated by immunological mechanisms ( i.e ., via the classic, lectin, or alternative pathway) (Ricklin et al ., 2010).”
Self-citationDewhirst, F. E., Chen, T., Izard, J., Paster, B. J., Tanner, A. C. R., Yu, W.-H., Lakshmanan, A., & Wade, W. G. (2010) · Journal of Bacteriology · doi:10.1128/jb.00542-10 · Cited by 3,352
The keystone-pathogen hypothesis
Hajishengallis, G., Darveau, R. P., & Curtis, M. A. (2012) · Nature Reviews Microbiology · doi:10.1038/nrmicro2873 · Cited by 1,790
Self-citationPeriodontitis: a polymicrobial disruption of host homeostasis
Darveau, R. P. (2010) · Nature Reviews Microbiology · doi:10.1038/nrmicro2337 · Cited by 1,688
Are dental diseases examples of ecological catastrophes?
Marsh, P. D. (2003) · Microbiology · doi:10.1099/mic.0.26082-0 · Cited by 1,256
Hajishengallis, G., Liang, S., Payne, M. A., Hashim, A., Jotwani, R., Eskan, M. A., McIntosh, M. L., Alsam, A., Kirkwood, K. L., Lambris, J. D., et al. (2011) · Cell Host & Microbe · doi:10.1016/j.chom.2011.10.006 · Cited by 1,154
Self-citationMetatranscriptomics of the Human Oral Microbiome during Health and Disease
Jorth, P., Turner, K. H., Gumus, P., Nizam, N., Buduneli, N., & Whiteley, M. (2014) · mBio · doi:10.1128/mbio.01012-14 · Cited by 386 · cited 2×
“…that periodontitis is not caused by a select few bacteria, historically referred to as ‘periopathogens’ (Abusleme et al ., 2013; Dewhirst et al ., 2010; Duran-Pinedo et al ., 2014; Griffen et al ., 2012; Hajishengallis et al ., 2011; Jiao et al ., 2013; Jorth et al ., 2014; Orth et al ., 2011).”
Community-wide transcriptome of the oral microbiome in subjects with and without periodontitis
Duran-Pinedo, A. E., Chen, T., Teles, R., Starr, J. R., Wang, X., Krishnan, K., & Frias-Lopez, J. (2014) · The ISME Journal · doi:10.1038/ismej.2014.23 · Cited by 327 · cited 2×
“Moreover, a plethora of virulence factors upregulated in the microbiome of periodontitis patients is primarily derived from species that are not traditionally considered as ‘periopathogens’ (Duran-Pinedo et al., 2014).”
Metabolite Cross-Feeding Enhances Virulence in a Model Polymicrobial Infection
Ramsey, M. M., Rumbaugh, K. P., & Whiteley, M. (2011) · PLoS Pathogens · doi:10.1371/journal.ppat.1002012 · Cited by 238
Cited by
Periodontitis: from microbial immune subversion to systemic inflammation
Hajishengallis, G. (2015) · Nature Reviews Immunology · doi:10.1038/nri3785 · Cited by 3,046
Self-citationThe Oral Microbiota: Dynamic Communities and Host Interactions
Lamont, R. J., Koo, H., & Hajishengallis, G. (2018) · Nature Reviews Microbiology · doi:10.1038/s41579-018-0089-x · Cited by 2,217
The oral microbiome – an update for oral healthcare professionals
Kilian, M., Chapple, I. L. C., Hannig, M., Marsh, P. D., Meuric, V., Pedersen, A. M. L., Tonetti, M. S., Wade, W. G., & Zaura, E. (2016) · British Dental Journal · doi:10.1038/sj.bdj.2016.865 · Cited by 1,269
Polymicrobial synergy and dysbiosis in inflammatory disease
Lamont, R. J., & Hajishengallis, G. (2015) · Trends in Molecular Medicine · doi:10.1016/j.molmed.2014.11.004 · Cited by 585
Self-citationGroeger, S., & Meyle, J. (2019) · Frontiers in Immunology · doi:10.3389/fimmu.2019.00208 · Cited by 473
Metadata
- Authors
- Hajishengallis, G.
- Venue
- Molecular Oral Microbiology
- Publisher
- Wiley
- Published
- 2014-09-08
- Volume
- 29
- Issue
- 6
- Pages
- 248-257
- ISSN
- 2041-1006 (ISSN-L)
- 2041-1014
- OpenAlex
- W2169722961
- Cited by
- 410
- References
- 9
- FWCI
- 31.73
- Type
- journal article
- Language
- en
- Open access
- bronze
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