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Porphyromonas gingivalis ‐induced production of reactive oxygen species, tumor necrosis factor‐α, interleukin‐6, CXCL 8 and CCL 2 by neutrophils from localized aggressive periodontitis and healthy donors: modulating actions of red blood cells and resolvin E1
Author(s) -
Damgaard C.,
Kantarci A.,
Holmstrup P.,
Hasturk H.,
Nielsen C. H.,
Van Dyke T. E.
Publication year - 2017
Publication title -
journal of periodontal research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.31
H-Index - 83
eISSN - 1600-0765
pISSN - 0022-3484
DOI - 10.1111/jre.12388
Subject(s) - porphyromonas gingivalis , chemokine , tumor necrosis factor alpha , proinflammatory cytokine , immunology , periodontitis , interleukin 8 , cytokine , chemistry , monocyte , chemotaxis , reactive oxygen species , ccl2 , inflammation , microbiology and biotechnology , biology , receptor , medicine , biochemistry
Background and Objectives Porphyromonas gingivalis is regarded as a significant contributor in the pathogenesis of periodontitis and certain systemic diseases, including atherosclerosis. P. gingivalis occasionally translocates from periodontal pockets into the circulation, where it adheres to red blood cells ( RBC s). This may protect the bacterium from contact with circulating phagocytes without affecting its viability. Material and Methods In this in vitro study, we investigated whether human peripheral blood neutrophils from 10 subjects with localized aggressive periodontitis ( LA gP) and 10 healthy controls release the proinflammatory cytokines interleukin ( IL )‐6, tumor necrosis factor α ( TNF ‐α), the chemokine (C‐X‐C motif) ligand 8 ( CXCL 8; also known as IL ‐8) and chemokine (C‐C motif) ligand 2 ( CCL 2; also known as monocyte chemotactic protein‐1) and intracellular reactive oxygen species ( ROS ) in response to challenge with P. gingivalis . In addition, the impact of RBC interaction with P. gingivalis was investigated. The actions of resolvin E1 (RvE1), a known regulator of P. gingivalis induced neutrophil responses, on the cytokine and ROS responses elicited by P. gingivalis in cultures of neutrophils were investigated. Results Upon stimulation with P. gingivalis , neutrophils from subjects with LA gP and healthy controls released similar quantities of IL ‐6, TNF ‐α, CXCL 8, CCL 2 and intracellular ROS . The presence of RBC s amplified the release of IL ‐6, TNF ‐α and CCL 2 statistically significant in both groups, but reduced the generation of ROS in the group of healthy controls, and showed a similar tendency in the group of subjects with LA gP. RvE1 had no impact on the production of intracellular ROS , TNF ‐α, IL ‐6, CXCL 8 and CCL 2 by neutrophils from either group, but tended to reduce the generation of ROS in subjects with LA gP in the absence of RBC s. Conclusions Our data support that binding to RBC s protects P. gingivalis from ROS and concomitantly enhances neutrophil release of proinflammatory cytokines providing a selective advantage for P. gingivalis growth.