Polymorphonuclear neutrophils in periodontitis and their possible modulation as a therapeutic approach

Nicu, Elena A.; Loos, Bruno G.

doi:10.1111/prd.12113

Cited by 46 publications

(49 citation statements)

References 222 publications

(241 reference statements)

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“…However as the system is always in some sort movement, it can swing into an aberrant immune function (one can observe this as an AgP case) or it can swing into a resolving or resolution phase (slow periodontal progression of many CP cases). Both the aberrant and resolution type host responses for periodontitis have been suggested in the literature (28,34,35). …”

Section: Periodontitis Development and Progressionmentioning

confidence: 99%

“…endotoxin, bacterial metabolic components), initiate the periodontal inflammatory reactions and these lead to the enhanced recruitment of polymorphonuclear neutrophilic granulocytes (PMN), and other inflammatory cells into the gingival tissues (28). Subsequently, the recruited immune cells, in particular PMN, but also the activated pocket epithelial cells and the fibroblasts in the underlying matrix, release pro-inflammatory mediators including cytokines, prostanoids and proteolytic enzymes (29).…”

Section: Periodontitis Development and Progressionmentioning

confidence: 99%

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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%

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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“…Pure populations of neutrophils are not usually encountered in vivo ; instead neutrophils are usually encountered as part of a heterogenous mixture of leukocytes and epithelial cells (Farrera and Fadeel, 2013; Heron et al, 2012; Nicu and Loos, 2016; Werner et al, 2011). Since these other cell types also express Fc receptors, pathogen recognition receptors, and/or selectins (Golebski et al, 2015; van Tongeren et al, 2015), we sought to determine whether the relationship described in Equation 1 could accurately measure neutrophil content in a heterogenous sample containing nasal epithelial cells.…”

Section: Resultsmentioning

confidence: 99%

“…During inflammation, neutrophils are recruited to the site of infections in response to elevated secretion of chemokines such as IL-8 and leukotrienes (Nicu and Loos, 2016) during the early, pro-inflammatory phase of an immune reaction. The later, resolving phases are characterized by the apoptosis and removal of neutrophils and increased production of anti-inflammatory factors such as IL-10 and TGFβ (Morris et al, 2015, 2014; Zhou et al, 2008).…”

Section: Discussionmentioning

confidence: 99%

“…They are the first cells recruited to the site of an infection or injury (Kolaczkowska and Kubes, 2013), constituting the “front line” of immune defense. Neutrophils migrate up concentration gradients of chemokines such as IL-8, before being arrested by selectins on the vascular endothelial surface and extravasating into tissue (Kobayashi, 2008; Nicu and Loos, 2016). During an active infection in mucosal tissues, resident innate cells such as macrophages effectively promote recruitment of neutrophils that are needed to clear infection (Farrera and Fadeel, 2013; Murray and Wynn, 2011).…”

Section: Introductionmentioning

confidence: 99%

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A PCR-based method for quantifying neutrophils in human nasal secretions

Morris

Khan

Pichichero

2017

Journal of Immunological Methods

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Neutrophil recruitment to the nasopharynx (NP) is a central event in resolution of NP-initiated microbial infections. A vigorous neutrophil response in infected tissues is also associated with the outcome of adverse tissue pathology. Therefore, differences in infection-induced tissue neutrophil numbers may correlate with pathogenesis events. Existing methods of quantifiying neutrophils require evaluation of NP samples within hours of procurement as flow cytometry based cell quantification methods require live neutrophil cells. Therefore, we developed a novel RT-PCR method that could reliably quantify neutrophil counts in frozen NP wash samples. mRNA transcripts of the genes encoding CD16, CD18, and CD62L were identified as neutrophil-specific in NP samples and not significantly variable in response to stimulation by heat killed bacteria, and can be used to derive an accurate assessment of neutrophil content in a sample even in the presence of epithelial cells. Using flow cytometry as a comparator, the method was validated in human NP wash samples. We conclude that this PCR-based method should prove useful for providing a quantitative estimate of neutrophil recruitment to the NP during infection and pathogenesis.

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Treponema denticola stimulates Oncostatin M cytokine release and de novo synthesis in neutrophils and macrophages

Jones

Vanyo

Ibraheem

et al. 2020

Journal of Leukocyte Biology

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Oncostatin M (OSM) is a pleiotropic cytokine elevated in a number of inflammatory conditions including periodontal disease. OSM is produced by a variety of immune cells and has diverse functionality such as regulation of metabolic processes, cell differentiation, and the inflammatory response to bacterial pathogens. The oral cavity is under constant immune surveillance including complementary neutrophil and macrophage populations, due to a persistent symbiotic bacterial presence. Periodontal disease is characterized by a dysbiotic bacterial community, with an abundance of Treponema denticola. Despite strong associations with severe periodontal disease, the source and mechanism of the release of OSM have not been defined in the oral cavity. We show that OSM protein is elevated in the gingival epithelium and immune cell infiltrate during periodontal disease. Furthermore, salivary and oral neutrophil OSM is elevated in correlation with the presence of T. denticola. In an air pouch infection model, T. denticola stimulated higher levels of OSM than the oral pathogen Porphorymonas gingivalis, despite differential recruitment of innate immune cells suggesting T. denticola has distinct properties to elevate OSM levels. OSM release and transcription were increased in isolated human blood, oral neutrophils, or macrophages exposed to T. denticola in vitro as measured by ELISA, qPCR, and microscopy. Using transcription, translation, and actin polymerization inhibition, we found that T. denticola stimulates both OSM release through degranulation and de novo synthesis in neutrophils and also OSM release and synthesis in macrophages. Differential induction of OSM by T. denticola may promote clinical periodontal disease.

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Polymorphonuclear neutrophils in periodontitis and their possible modulation as a therapeutic approach

Cited by 46 publications

References 222 publications

What is the Contribution of Genetics to Periodontal Risk?

What is the Contribution of Genetics to Periodontal Risk?

A PCR-based method for quantifying neutrophils in human nasal secretions

Treponema denticola stimulates Oncostatin M cytokine release and de novo synthesis in neutrophils and macrophages

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