Vesicular Messages from Dental Biofilms for Neutrophils

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dc.citation.spage3314
dc.citation.volume25
dc.contributor.authorVitkov, Ljubomir
dc.contributor.authorKrunić, Jelena
dc.contributor.authorDudek, Johanna
dc.contributor.authorReddy Bobbili, Madhusudhan
dc.contributor.authorGrillari, Johannes
dc.contributor.authorHausegger, Bernhard
dc.contributor.authorMladenović, Irena
dc.contributor.authorStojanović, Nikola
dc.contributor.authorDietrich Krautgartner, Wolf
dc.contributor.authorOberthaler, Hannah
dc.contributor.authorSchauer, Christine
dc.contributor.authorHerrmann, Martin
dc.contributor.authorSingh, Jeeshan
dc.contributor.authorMinnich, Bernd
dc.contributor.authorHannig, Matthias
dc.date.accessioned2024-11-08T12:15:18Z
dc.date.available2024-11-08T12:15:18Z
dc.date.issued2024
dc.description.abstractThe encounter between dental biofilm and neutrophils in periodontitis remains elusive, although it apparently plays a crucial role in the periodontal pathology and constitutes a key topic of periodontology. Dental biofilm and neutrophils were isolated from orally healthy persons and patients with periodontitis. We investigated biofilm and its particle-shedding phenomenon with electron microscopy and nanoparticle tracking analysis (NTA); biofilm shedding–neutrophil interactions were examined ex vivo with epi-fluorescence microscopy. For this purpose, we used acellular dental biofilm shedding, purified lipopolysaccharide (LPS), and phorbol 12-myristate 13-acetate (PMA) as activators, and the interleukin 8 receptor beta (CXCR2) inhibitor and the anti-interleukin 8 receptor alpha (CXCR1) antibody as modulators. The shedding of acellular dental biofilms overwhelmingly consists of bacterial extracellular vesicles (BEVs). The latter induced the moderate formation of neutrophil extracellular traps (NETs) in orally healthy subjects and a strong formation in patients with periodontitis. A CXCR2 inhibitor and an anti-CXCR1 antibody had a minor effect on NET formation. Neutrophils from patients with periodontitis exhibited NET hyper-responsiveness. BEVs were stronger inducers of NET formation than purified LPS and PMA. A plateau of neutrophil responsiveness is reached above the age of 40 years, indicating the abrupt switch of maladaptive trained immunity (TI) into the activated modus. Our results suggest that dental biofilms consist of and disseminate immense amounts of outer membrane vesicles (OMVs), which initiate NET formation via a non-canonical cytosolic LPS/caspase-4/11/Gasdermin D pathway. This modus of NET formation is independent of neutrophil elastase (NE), myeloperoxidase (MPO), peptidylarginine deiminase 4 (PAD4), and toll-like receptors (TLR). In periodontitis, the hyper-responsiveness of neutrophils to BEVs and the increased NET formation appear to be a consequence of TI.
dc.identifier.doi10.3390/ijms25063314
dc.identifier.urihttps://vaseljena.ues.rs.ba/handle/123456789/1260
dc.language.isoen
dc.publisherMDPI
dc.sourceInternational Journal o f Molecular Sciences
dc.subjectperiodontitis; dental biofilm; bacterial extracellular vesicles; outer membrane vesicles; caspase 4; trained immunity
dc.titleVesicular Messages from Dental Biofilms for Neutrophils
dc.typeArticle
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