Periodontal Pathogens’ strategies disarm neutrophils to promote dysregulated inflammation

Abstract

Periodontal diseases affect the integrity of one or several tissues of the periodontium, which is comprised of the gingiva, periodontal ligament, cementum, and alveolar bone. Periodontitis is an irreversible, chronic inflammatory disease that causes the loss of connective tissue, alveolar bone, and eventually the loss of teeth (Pihlstrom et al., 2005). Preventative and treatment measures aim to control or

Interactions Between Neutrophils and Periodontal Pathogens in Late-Onset Periodontitis

“…These findings indicate that F. alocis-mediated inhibition of ROS generation is not a global mechanism but a local phagosomal mechanism. As discussed above, prior to generating ROS, NADPH oxidase components are recruited, assembling at phagosome membrane and/or plasma membrane (Miralda and Uriarte, 2020). Therefore, phagosomes containing F. alocis might prevent NADPH oxidase recruitment, but the exact mechanism warrants further studies.…”

“…In resting neutrophils, the NADPH oxidase complex is unassembled and inactive. Upon stimulation, these separate components translocate to the membrane to form the enzyme complex with a catalytic activity (Groemping et al, 2003;Nauseef, 2019;Miralda and Uriarte, 2020). The generated ROS can be released into the extracellular space or into the phagosome according to the stimulus.…”

“…When encountered with a soluble stimulus, the NADPH oxidase complex assembles on the plasma membrane, and the generated ROS is released into the extracellular space. When faced with a particulate stimulus, such as a pathogen, the NADPH oxidase complex assembles on the particle-containing phagosome membrane, and the generated ROS is released into the phagosome (Miralda and Uriarte, 2020). ROS can cause direct oxidative damage to microbes, such as oxidation of methionine residues, lipid peroxidation, base oxidation and deamination, and DNA strand breakage (Paiva and Bozza, 2014).…”

“…Moreover, the supernatants of P. gingivalis and F. nucleatum can inhibit fMLP-induced chemotaxis by binding nonchemotactic bacterial peptides to fMLP receptors, making neutrophils unable to detect the chemotactic gradient (Van Dyke et al, 1982;Miralda and Uriarte, 2020). It has also been reported that oral neutrophils express fewer fMLP receptors, and their directional movement toward fMLP is impaired; However, the effect of periodontal pathogens on the downregulation of fMLP receptors expression on neutrophils is unclear (Moonen et al, 2019).…”

How Do Polymer Coatings Affect the Growth and Bacterial Population of a Biofilm Formed by Total Human Salivary Bacteria?—A Study by 16S-RNA Sequencing

“…Gram− facultative anaerobe associated with peridodontitis. [9,10] Brevundimonas diminuta Gram− aerobe periodontal pathogen, in subgingival niche [37] Campylobacter consisus Gram− anaerobe in subgingival niche, isolated from the oral cavity of patients with gingivitis and periodontitis, but with no clear association to either disease or other human oral inflammatory diseases [38] Campylobacter curvus Gram− anaerobe subgingival; no significant evidence for causing periodontal disease, but found it higher proportions at periodontitis sites as compared to healthy ones [39] Campylobacter ureolyticus Gram− anaerobe gastrointestinal pathogen; present in subgingival plaque; associated with poor oral hygiene. [40] Corynebacterium Gram+ aerobe, facultative anaerobe found in dental plaque, associated with the formation of dental calculi [41] Dialister Gram− anaerobe D. pneumosintes and D. invisus are periodontal pathogens, have been associated with refractory periodontitis, acute necrotizing ulcerative gingivitis, endodontic infections; subgingival [37,42] Enterococcus Gram+ anaerobe E. faecalis has been related to caries, endodontic infections, periodontitis, and peri-implantitis, biofilm former able to integrate in the oral biofilm in situ [43] Filifactor alocis Gram+ anaerobe associated with periodontitis.…”