NETs Are Double-Edged Swords with the Potential to Aggravate or Resolve Periodontal Inflammation

Vitkov, Ljubomir; Minnich, Bernd; Knopf, Jasmin; Schauer, Christine; Hannig, Matthias; Herrmann, Martin

doi:10.3390/cells9122614

Cited by 19 publications

(18 citation statements)

References 139 publications

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“…The formation of periodontal pockets is the most important pathological change of CP when swelling or hyperplasia of the gingiva deepens the position of the gingival margin toward the crown, but the epithelium proliferates toward the root making the crown part (the bottom of the gingival sulcus) separate from the tooth surface to form periodontal pockets. 21 Plaque and tartar in the periodontal pocket cause mechanical damage to the soft tissues of the periodontal pocket wall and caused bleeding in the pocket. 22 Therefore, probing pocket depth and attachment loos are known to be the main features of the periodontal tissue destruction index, 23 and they are crucial indicators for the diagnosis of CP along with plaque index and bleeding index, which can represent its severity and progression.…”

Section: Discussionmentioning

confidence: 99%

MicroRNA-28-5p as a potential diagnostic biomarker for chronic periodontitis and its role in cell proliferation and inflammatory response

Huang

Jia

2022

Journal of Dental Sciences

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Section: Discussionmentioning

confidence: 99%

MicroRNA-28-5p as a potential diagnostic biomarker for chronic periodontitis and its role in cell proliferation and inflammatory response

Huang

Jia

2022

Journal of Dental Sciences

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“…Calprotectin heterotetramers also lose DAMP activity because this multimer shows reduced access to the TLR4/MD2-binding site, which mitigates a broader inflammatory response [ 199 ]. By reducing the inflammatory response, off-target tissue damage is minimized during clearance of the infection [ 200 – 203 ].…”

Section: Calprotectin As a Location-dependent Ampmentioning

confidence: 99%

Antimicrobial peptides: Defending the mucosal epithelial barrier

Johnstone

Herzberg

2022

Front. Oral. Health

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The recent epidemic caused by aerosolized SARS-CoV-2 virus illustrates the importance and vulnerability of the mucosal epithelial barrier against infection. Antimicrobial proteins and peptides (AMPs) are key to the epithelial barrier, providing immunity against microbes. In primitive life forms, AMPs protect the integument and the gut against pathogenic microbes. AMPs have also evolved in humans and other mammals to enhance newer, complex innate and adaptive immunity to favor the persistence of commensals over pathogenic microbes. The canonical AMPs are helictical peptides that form lethal pores in microbial membranes. In higher life forms, this type of AMP is exemplified by the defensin family of AMPs. In epithelial tissues, defensins, and calprotectin (complex of S100A8 and S100A9) have evolved to work cooperatively. The mechanisms of action differ. Unlike defensins, calprotectin sequesters essential trace metals from microbes, which inhibits growth. This review focuses on defensins and calprotectin as AMPs that appear to work cooperatively to fortify the epithelial barrier against infection. The antimicrobial spectrum is broad with overlap between the two AMPs. In mice, experimental models highlight the contribution of both AMPs to candidiasis as a fungal infection and periodontitis resulting from bacterial dysbiosis. These AMPs appear to contribute to innate immunity in humans, protecting the commensal microflora and restricting the emergence of pathobionts and pathogens. A striking example in human innate immunity is that elevated serum calprotectin protects against neonatal sepsis. Calprotectin is also remarkable because of functional differences when localized in epithelial and neutrophil cytoplasm or released into the extracellular environment. In the cytoplasm, calprotectin appears to protect against invasive pathogens. Extracellularly, calprotectin can engage pathogen-recognition receptors to activate innate immune and proinflammatory mechanisms. In inflamed epithelial and other tissue spaces, calprotectin, DNA, and histones are released from degranulated neutrophils to form insoluble antimicrobial barriers termed neutrophil extracellular traps. Hence, calprotectin and other AMPs use several strategies to provide microbial control and stimulate innate immunity.

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“…The formation of periodontal pockets interferes with the clearance of pathogenassociated molecular patterns (PAMPs) and damage-associated molecular patterns (DAMPs). These PAMPs and DAMPs trigger excessive NET formation, inducing tissue damage and progression of periodontitis (Vitkov et al, 2017;Vitkov et al, 2020).…”

Section: Net Formationmentioning

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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NETs Are Double-Edged Swords with the Potential to Aggravate or Resolve Periodontal Inflammation

Cited by 19 publications

References 139 publications

MicroRNA-28-5p as a potential diagnostic biomarker for chronic periodontitis and its role in cell proliferation and inflammatory response

MicroRNA-28-5p as a potential diagnostic biomarker for chronic periodontitis and its role in cell proliferation and inflammatory response

Antimicrobial peptides: Defending the mucosal epithelial barrier

Interactions Between Neutrophils and Periodontal Pathogens in Late-Onset Periodontitis

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