Polymicrobial synergy and dysbiosis in inflammatory disease

Lamont, Richard J.; Hajishengallis, George

doi:10.1016/j.molmed.2014.11.004

Cited by 445 publications

(485 citation statements)

References 90 publications

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“…In mathematical terms, the bacteria of the subgingival biofilms come into contact with the host defense elements through random walk and beyond a criticality in their interaction, the confrontation of bacteria to the host defense is driven out of equilibrium. Interestingly, it has been proposed that there are keystone pathogens that elevate community virulence and the resulting dysbiotic community targets specific aspects of host immunity promoting an aberrant immune response (31). At this point, self-organization (SO) of the host defense system occurs (32).…”

Section: Periodontitis Development and Progressionmentioning

confidence: 99%

What is the Contribution of Genetics to Periodontal Risk?

Loos

Papantonopoulos

Jepsen

et al. 2015

Dental Clinics of North America

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This review addresses the multi-causal etiology of periodontitis, in which genetic factors play a role. The various proposed causes for periodontitis always play a role simultaneously, but the relative contribution of each of these, varies from case to case. In young individuals often with aggressive periodontitis (AgP) a stronger contribution from genetic factors is apparent, while in older individuals often with chronic periodontitis (CP), the relative contribution of the established subgingival biofilms (environmental factors) and life style factors (e.g. smoking, stress, diet), play a more dominant role in the phenotype of the disease.Nevertheless always some genetic susceptibility is present, for CP estimated at 25%.Periodontitis is therefore a complex disease, i.e. it behaves in a nonlinear fashion. Actually the disease progression rate fluctuates, where the disease sometimes moves into an aberrant state of host response and then swings back into a resolving state; in between, a settlement zone is present where essentially no differences are found for immunological parameters between cases with periodontitis and healthy controls. The genotype determines part of this fluctuation and the extent of it. The disease is polygenic, i.e. multiple genetic variants in multiple genes determine the phenotype, but there are individual and ethnic differences in the genes involved. We are still at the early stage to have identified the involved genes, in comparisons to other chronic diseases, we need to count on it that at least 100 causative genes across various global populations exist in AgP and CP. To date, the genetic variations firmly and repeatedly associated with periodontitis in some populations are found within the following genes: ANRIL, COX2, IL1, IL10, DEFB1, while many proposed periodontitis candidate genes have not been firmly proven or replicated. 3 KeypointsPeriodontitis is a multi-causal disease, with each of the causal factors playing a role but the relative contribution of these vary form case to case.The disease behaves in a nonlinear fashion, with periods of aberrant host response to periods within an active disease resolving state.To date only a few of the multitude of possible genetic factors for periodontitis are identified. Outline

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Section: Periodontitis Development and Progressionmentioning

confidence: 99%

What is the Contribution of Genetics to Periodontal Risk?

Loos

Papantonopoulos

Jepsen

et al. 2015

Dental Clinics of North America

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“…Periodontitis is characterized as a polymicrobial disease that involves dysbiosis of the indigenous flora in the subgingival biofilm. 1 Among the more than 500 bacterial species harbored in the subgingival biofilm, Porphyromonas gingivalis, Treponema denticola, and Tannerella forsythia are well-characterized periodontal pathogens. 2 P. gingivalis, a gram-negative obligate anaerobe, has a number of virulence factors such as cysteine proteases (gingipains), major fimbriae, lipopolysaccharide, and capsule.…”

Section: Introductionmentioning

confidence: 99%

Association of the invasion ability ofPorphyromonas gingivaliswith the severity of periodontitis

Baek

Ji²,

Kim

et al. 2015

Virulence

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(2015) Association of the invasion ability of Porphyromonasgingivalis with the severity of periodontitis, Virulence, 6:3, 274-281, DOI: 10.1080/21505594.2014 Keywords: cytokine proteolytic activity, invasion ability, Porphyromonas gingivalis, periodontitis, severityPorphyromonas gingivalis is one of the well-characterized periodontal pathogens involved in periodontitis. The invasive and proteolytic activities of P. gingivalis clinical isolates have been shown to be associated with heterogenic virulence, as determined in a mouse abscess model. The aims of the present study were to identify a P. gingivalis strain with a low virulence among clinical isolates, based on its invasive ability and cytokine proteolytic activities, and to explore the preferential degradation of a certain cytokine by P. gingivalis. P. gingivalis ATCC 33277, W50, and 10 clinical isolates were used. After incubating bacteria with IL-4, IL-6, IL-10, IL-17A, TNFa, IFNg, and IL-1a, the amounts of remaining cytokines were determined by ELISA. Invasion ability was measured by a flow cytometric invasion assay. There was inter-strain variability both in the cytokine proteolytic activities and invasion ability. In addition, differential degradation of cytokines by P. gingivalis was observed: while IFNg and IL-17A were almost completely degraded, inflammatory cytokines TNFa and IL-1a were less susceptible to degradation. Interestingly, the invasion index, but not cytokine proteolytic activities, of P. gingivalis had strong positive correlations with clinical parameters of subjects who harbored the isolates. Therefore, the invasive ability of P. gingivalis is an important virulence factor, and the bacterial invasion step may be a good target for new therapeutics of periodontitis.

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“…Also genetic, environmental and various other acquired factors influence this process such that the clinical scenario observed is a summation of all the factors taken together. The disease severity and progression itself can alter the clinical picture by giving a feedback in terms of environment alteration like availability of various nutrients or oxygen [10].…”

Section: Risk Factors Of Periodontitismentioning

confidence: 99%

Periodontitis- A Review

Shah¹

2017

Med Clin Rev

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The early form of periodontitis is gingivitis where inflammatory changes including bleeding and swelling are restricted to marginal gingiva and surrounding connective tissue, without the involvement of periodontal ligament. Periodontitis occurs when inflammatory changes reach the periodontal ligament and alveolar bone ultimately leading to tooth loss. The underlying cause of the disease is the presence of a polymicrobial biofilm that forms as plaque on the tooth surface and the resulting host response that this plaque induces. Inflammatory responses are initiated by a number of late stage colonizers and the virulence factors they produce. Among these late stage pathogens is P. gingivalis, a Gram negative, asacchrolytic bacterium with a large arsenal of virulence factors. P. gingivalis produces up to 13 virulence factors involved in host evasion and 21 virulence factors involved in tissue destruction. The presence of these virulence factors induces the production of proinflammatory chemokine and cytokine responses often seen in the saliva and gingival crevicular fluid of individuals with periodontitis.

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Polymicrobial synergy and dysbiosis in inflammatory disease

Cited by 445 publications

References 90 publications

What is the Contribution of Genetics to Periodontal Risk?

What is the Contribution of Genetics to Periodontal Risk?

Association of the invasion ability ofPorphyromonas gingivaliswith the severity of periodontitis

Periodontitis- A Review

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