Neutrophil Extracellular Traps in Periodontitis

Magán‐Fernández, Antonio; Al-Bakri, Sarmad Muayad Rasheed; O’Valle, Francisco; Benavides-Reyes, Cristina; Abadía-Molina, Francisco; Mesa, Francisco

doi:10.3390/cells9061494

Cited by 53 publications

(59 citation statements)

References 104 publications

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“…Next, Estúa-Acosta et al challenge the idea that the eye is an immune-privileged organ and provide evidence of NETs and their implication in pathophysiology in infectious keratitis, the leading cause of monocular blindness as well as non-infectious eye diseases [ 9 ]. Meanwhile, Magán-Fernández et al summarize the current knowledge about the role of NETs in the pathogenesis of periodontitis [ 10 ]. Infection of the periodontium starts with the accumulation of a complex bacterial biofilm that induces dysbiosis between the gingival microbiome and the immune response of the host, which involves impaired NET formation and/or elimination [ 10 ].…”

Section: Neutrophils and Nets In Infectionmentioning

confidence: 99%

“…Meanwhile, Magán-Fernández et al summarize the current knowledge about the role of NETs in the pathogenesis of periodontitis [ 10 ]. Infection of the periodontium starts with the accumulation of a complex bacterial biofilm that induces dysbiosis between the gingival microbiome and the immune response of the host, which involves impaired NET formation and/or elimination [ 10 ]. Furthermore, the formation of biofilms promotes the efficient growth of pathogenic bacteria and fungi by providing optimal local environmental conditions and increased protection against the immune system [ 11 ].…”

Section: Neutrophils and Nets In Infectionmentioning

confidence: 99%

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Neutrophils and Neutrophil Extracellular Traps Regulate Immune Responses in Health and Disease

Mulay

Anders

2020

Cells

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Section: Neutrophils and Nets In Infectionmentioning

confidence: 99%

Section: Neutrophils and Nets In Infectionmentioning

confidence: 99%

Neutrophils and Neutrophil Extracellular Traps Regulate Immune Responses in Health and Disease

Mulay

Anders

2020

Cells

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“…However, a study showed that aggregated NETs could resolve inflammation by the proteolysis of cytokines and chemokines ( Hahn et al., 2019 ). Current evidence also suggests that NETs contribute to many diseases like thrombosis ( Kimball et al., 2016 ), atherosclerosis ( Franck et al., 2018 ), autoimmune diseases ( Frangou et al., 2019a ; Frangou et al., 2019b ), sepsis ( Denning et al., 2019 ), and periodontitis ( Magan-Fernandez et al., 2020 ).…”

Section: Introductionmentioning

confidence: 99%

The Role of Neutrophil Extracellular Traps in Periodontitis

Wang

Zhou

Ren

et al. 2021

Front. Cell. Infect. Microbiol.

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Periodontitis is a chronic, destructive disease of periodontal tissues caused by multifaceted, dynamic interactions. Periodontal bacteria and host immunity jointly contribute to the pathological processes of the disease. The dysbiotic microbial communities elicit an excessive immune response, mainly by polymorphonuclear neutrophils (PMNs). As one of the main mechanisms of PMN immune response in the oral cavity, neutrophil extracellular traps (NETs) play a crucial role in the initiation and progression of late-onset periodontitis. NETs are generated and released by neutrophils stimulated by various irritants, such as pathogens, host-derived mediators, and drugs. Chromatin and proteins are the main components of NETs. Depending on the characteristics of the processes, three main pathways of NET formation have been described. NETs can trap and kill pathogens by increased expression of antibacterial components and identifying and trapping bacteria to restrict their spread. Moreover, NETs can promote and reduce inflammation, inflicting injuries on the tissues during the pro-inflammation process. During their long-term encounter with NETs, periodontal bacteria have developed various mechanisms, including breaking down DNA of NETs, degrading antibacterial proteins, and impacting NET levels in the pocket environment to resist the antibacterial function of NETs. In addition, periodontal pathogens can secrete pro-inflammatory factors to perpetuate the inflammatory environment and a friendly growth environment, which are responsible for the progressive tissue damage. By learning the strategies of pathogens, regulating the periodontal concentration of NETs becomes possible. Some practical ways to treat late-onset periodontitis are reducing the concentration of NETs, administering anti-inflammatory therapy, and prescribing broad-spectrum and specific antibacterial agents. This review mainly focuses on the mechanism of NETs, pathogenesis of periodontitis, and potential therapeutic approaches based on interactions between NETs and periodontal pathogens.

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“…Neutrophils in periodontitis also have a higher cytokine reactivity as the expression of chemokines and the release of cytokines (IL-1b, IL-6, IL-8, and TNF-a) are higher in neutrophils isolated from late-onset periodontitis patients (Lakschevitz et al, 2013;Ling et al, 2015). However, during periodontitis, the immune response is a double-edged sword because the cytokines and antimicrobial components produced during the immune response, such as IL-17, IL-6, IL-1b, TNF-a, ROS, and NETs, can induce bone resorption and soft tissue injury (Ramadan et al, 2020;Magan-Fernandez et al, 2020). In periodontitis, neutrophils are recruited through tethering and rolling, adhesion, crawling, and transmigration.…”

Section: Introductionmentioning

confidence: 99%

Interactions Between Neutrophils and Periodontal Pathogens in Late-Onset Periodontitis

Jiang

Zhao

Shui

et al. 2021

Front. Cell. Infect. Microbiol.

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Late-onset periodontitis is associated with a series of inflammatory reactions induced by periodontal pathogens, such as Porphyromonas gingivalis, a keystone pathogen involved in periodontitis. Neutrophils are the most abundant leukocytes in the periodontal pocket/gingival crevice and inflamed periodontal tissues. They form a “wall” between the dental plaque and the junctional epithelium, preventing microbial invasion. The balance between neutrophils and the microbial community is essential to periodontal homeostasis. Excessive activation of neutrophils in response to periodontal pathogens can induce tissue damage and lead to periodontitis persistence. Therefore, illuminating the interactions between neutrophils and periodontal pathogens is critical for progress in the field of periodontitis. The present review aimed to summarize the interactions between neutrophils and periodontal pathogens in late-onset periodontitis, including neutrophil recruitment, neutrophil mechanisms to clear the pathogens, and pathogen strategies to evade neutrophil-mediated elimination of bacteria. The recruitment is a multi-step process, including tethering and rolling, adhesion, crawling, and transmigration. Neutrophils clear the pathogens mainly by phagocytosis, respiratory burst responses, degranulation, and neutrophil extracellular trap (NET) formation. The mechanisms that pathogens activate to evade neutrophil-mediated killing include impairing neutrophil recruitment, preventing phagocytosis, uncoupling killing from inflammation, and resistance to ROS, degranulation products, and NETs.

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Neutrophil Extracellular Traps in Periodontitis

Cited by 53 publications

References 104 publications

Neutrophils and Neutrophil Extracellular Traps Regulate Immune Responses in Health and Disease

Neutrophils and Neutrophil Extracellular Traps Regulate Immune Responses in Health and Disease

The Role of Neutrophil Extracellular Traps in Periodontitis

Interactions Between Neutrophils and Periodontal Pathogens in Late-Onset Periodontitis

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