{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,10]],"date-time":"2026-10-10T18:59:09Z","timestamp":1791658749820,"version":"4.3.4"},"reference-count":55,"publisher":"Wiley","issue":"2","license":[{"start":{"date-parts":[[2016,5,5]],"date-time":"2016-05-05T00:00:00Z","timestamp":1462406400000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"funder":[{"DOI":"10.13039\/100008364","name":"Tandl\u00e6geforeningen","doi-asserted-by":"publisher","id":[{"id":"10.13039\/100008364","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000072","name":"National Institute of Dental and Craniofacial Research","doi-asserted-by":"publisher","id":[{"id":"10.13039\/100000072","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["J of Periodontal Research"],"published-print":{"date-parts":[[2017,4]]},"abstract":"<jats:sec><jats:title>Background and Objectives<\/jats:title><jats:p><jats:italic>Porphyromonas gingivalis<\/jats:italic> is regarded as a significant contributor in the pathogenesis of periodontitis and certain systemic diseases, including atherosclerosis. <jats:italic>P.\u00a0gingivalis<\/jats:italic> occasionally translocates from periodontal pockets into the circulation, where it adheres to red blood cells (<jats:styled-content style=\"fixed-case\">RBC<\/jats:styled-content>s). This may protect the bacterium from contact with circulating phagocytes without affecting its viability.<\/jats:p><\/jats:sec><jats:sec><jats:title>Material and Methods<\/jats:title><jats:p>In this <jats:italic>in vitro<\/jats:italic> study, we investigated whether human peripheral blood neutrophils from 10 subjects with localized aggressive periodontitis (<jats:styled-content style=\"fixed-case\">LA<\/jats:styled-content>gP) and 10 healthy controls release the proinflammatory cytokines interleukin (<jats:styled-content style=\"fixed-case\">IL<\/jats:styled-content>)\u20106, tumor necrosis factor \u03b1 (<jats:styled-content style=\"fixed-case\">TNF<\/jats:styled-content>\u2010\u03b1), the chemokine (C\u2010X\u2010C motif) ligand 8 (<jats:styled-content style=\"fixed-case\">CXCL<\/jats:styled-content>8; also known as <jats:styled-content style=\"fixed-case\">IL<\/jats:styled-content>\u20108) and chemokine (C\u2010C motif) ligand 2 (<jats:styled-content style=\"fixed-case\">CCL<\/jats:styled-content>2; also known as monocyte chemotactic protein\u20101) and intracellular reactive oxygen species (<jats:styled-content style=\"fixed-case\">ROS<\/jats:styled-content>) in response to challenge with <jats:italic>P.\u00a0gingivalis<\/jats:italic>. In addition, the impact of <jats:styled-content style=\"fixed-case\">RBC<\/jats:styled-content> interaction with <jats:italic>P.\u00a0gingivalis<\/jats:italic> was investigated. The actions of resolvin E1 (RvE1), a known regulator of <jats:italic>P.\u00a0gingivalis<\/jats:italic> induced neutrophil responses, on the cytokine and <jats:styled-content style=\"fixed-case\">ROS<\/jats:styled-content> responses elicited by <jats:italic>P.\u00a0gingivalis<\/jats:italic> in cultures of neutrophils were investigated.<\/jats:p><\/jats:sec><jats:sec><jats:title>Results<\/jats:title><jats:p>Upon stimulation with <jats:italic>P.\u00a0gingivalis<\/jats:italic>, neutrophils from subjects with <jats:styled-content style=\"fixed-case\">LA<\/jats:styled-content>gP and healthy controls released similar quantities of <jats:styled-content style=\"fixed-case\">IL<\/jats:styled-content>\u20106, <jats:styled-content style=\"fixed-case\">TNF<\/jats:styled-content>\u2010\u03b1, <jats:styled-content style=\"fixed-case\">CXCL<\/jats:styled-content>8, <jats:styled-content style=\"fixed-case\">CCL<\/jats:styled-content>2 and intracellular <jats:styled-content style=\"fixed-case\">ROS<\/jats:styled-content>. The presence of <jats:styled-content style=\"fixed-case\">RBC<\/jats:styled-content>s amplified the release of <jats:styled-content style=\"fixed-case\">IL<\/jats:styled-content>\u20106, <jats:styled-content style=\"fixed-case\">TNF<\/jats:styled-content>\u2010\u03b1 and <jats:styled-content style=\"fixed-case\">CCL<\/jats:styled-content>2 statistically significant in both groups, but reduced the generation of <jats:styled-content style=\"fixed-case\">ROS<\/jats:styled-content> in the group of healthy controls, and showed a similar tendency in the group of subjects with <jats:styled-content style=\"fixed-case\">LA<\/jats:styled-content>gP. RvE1 had no impact on the production of intracellular <jats:styled-content style=\"fixed-case\">ROS<\/jats:styled-content>,<jats:styled-content style=\"fixed-case\"> TNF<\/jats:styled-content>\u2010\u03b1, <jats:styled-content style=\"fixed-case\">IL<\/jats:styled-content>\u20106, <jats:styled-content style=\"fixed-case\">CXCL<\/jats:styled-content>8 and <jats:styled-content style=\"fixed-case\">CCL<\/jats:styled-content>2 by neutrophils from either group, but tended to reduce the generation of <jats:styled-content style=\"fixed-case\">ROS<\/jats:styled-content> in subjects with <jats:styled-content style=\"fixed-case\">LA<\/jats:styled-content>gP in the absence of <jats:styled-content style=\"fixed-case\">RBC<\/jats:styled-content>s.<\/jats:p><\/jats:sec><jats:sec><jats:title>Conclusions<\/jats:title><jats:p>Our data support that binding to <jats:styled-content style=\"fixed-case\">RBC<\/jats:styled-content>s protects <jats:italic>P.\u00a0gingivalis<\/jats:italic> from <jats:styled-content style=\"fixed-case\">ROS<\/jats:styled-content> and concomitantly enhances neutrophil release of proinflammatory cytokines providing a selective advantage for <jats:italic>P.\u00a0gingivalis<\/jats:italic> growth.<\/jats:p><\/jats:sec>","DOI":"10.1111\/jre.12388","type":"journal-article","created":{"date-parts":[[2016,5,5]],"date-time":"2016-05-05T11:47:17Z","timestamp":1462448837000},"page":"246-254","source":"Crossref","is-referenced-by-count":40,"title":["<i>Porphyromonas gingivalis<\/i>\u2010induced production of reactive oxygen species, tumor necrosis factor\u2010\u03b1, interleukin\u20106, <scp>CXCL<\/scp>8 and <scp>CCL<\/scp>2 by neutrophils from localized aggressive periodontitis and healthy donors: modulating actions of red blood cells and resolvin E1"],"prefix":"10.1111","volume":"52","author":[{"given":"C.","family":"Damgaard","sequence":"first","affiliation":[{"name":"Section for Periodontology, Microbiology and Community Dentistry Department of Odontology Faculty of Health and Medical Sciences University of Copenhagen Copenhagen Denmark"},{"name":"Institute for Inflammation Research Center for Rheumatology and Spine Disease Rigshospitalet Copenhagen University Hospital Copenhagen Denmark"},{"name":"Department of Applied Oral Sciences Center for Periodontology The Forsyth Institute Cambridge MA USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"A.","family":"Kantarci","sequence":"additional","affiliation":[{"name":"Department of Applied Oral Sciences Center for Periodontology The Forsyth Institute Cambridge MA USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"P.","family":"Holmstrup","sequence":"additional","affiliation":[{"name":"Section for Periodontology, Microbiology and Community Dentistry Department of Odontology Faculty of Health and Medical Sciences University of Copenhagen Copenhagen Denmark"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"H.","family":"Hasturk","sequence":"additional","affiliation":[{"name":"Department of Applied Oral Sciences Center for Periodontology The Forsyth Institute Cambridge MA USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"C. 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