Impaired Phagocytosis in Localized Aggressive Periodontitis: Rescue by Resolvin E1
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[1] C. Serhan,et al. Metabolomics‐Lipidomics of Eicosanoids and Docosanoids Generated by Phagocytes , 2011, Current protocols in immunology.
[2] C. Serhan,et al. Pro-resolving actions and stereoselective biosynthesis of 18S E-series resolvins in human leukocytes and murine inflammation. , 2011, The Journal of clinical investigation.
[3] A. Kantarcı,et al. Adjunctive treatment of chronic periodontitis with daily dietary supplementation with omega-3 Fatty acids and low-dose aspirin. , 2010, Journal of periodontology.
[4] G. Davı̀,et al. Cystic fibrosis transmembrane conductance regulator (CFTR) expression in human platelets: impact on mediators and mechanisms of the inflammatory response , 2010, FASEB journal : official publication of the Federation of American Societies for Experimental Biology.
[5] C. Serhan,et al. Resolvin D1 binds human phagocytes with evidence for proresolving receptors , 2010, Proceedings of the National Academy of Sciences.
[6] I. Tabas. Macrophage death and defective inflammation resolution in atherosclerosis , 2010, Nature Reviews Immunology.
[7] J. Takeda,et al. The Anti-Inflammatory and Proresolving Mediator Resolvin E1 Protects Mice from Bacterial Pneumonia and Acute Lung Injury , 2009, The Journal of Immunology.
[8] C. Serhan,et al. Resolvin E1 Receptor Activation Signals Phosphorylation and Phagocytosis* , 2009, The Journal of Biological Chemistry.
[9] P. Libby,et al. The American Journal of Cardiology and Journal of Periodontology editors' consensus: periodontitis and atherosclerotic cardiovascular disease. , 2009, Journal of periodontology.
[10] J. Walters,et al. Neutrophil formylpeptide receptor single nucleotide polymorphism 348T>C in aggressive periodontitis. , 2009, Journal of periodontology.
[11] R. Nieuwland,et al. Elevated platelet and leukocyte response to oral bacteria in periodontitis , 2009, Journal of thrombosis and haemostasis : JTH.
[12] C. Serhan,et al. Atherosclerosis: evidence for impairment of resolution of vascular inflammation governed by specific lipid mediators , 2008, FASEB journal : official publication of the Federation of American Societies for Experimental Biology.
[13] J. Schwab,et al. Resolvin E1, an EPA-derived mediator in whole blood, selectively counterregulates leukocytes and platelets. , 2008, Blood.
[14] B. Levy,et al. Resolvin E1 regulates interleukin 23, interferon-γ and lipoxin A4 to promote the resolution of allergic airway inflammation , 2008, Nature Immunology.
[15] C. Andry,et al. Resolvin E1 Regulates Inflammation at the Cellular and Tissue Level and Restores Tissue Homeostasis In Vivo1 , 2007, The Journal of Immunology.
[16] P. Eke,et al. Case Definitions for Use in Population-Based Surveillance of Periodontitis. , 2007, Journal of periodontology.
[17] Charles N. Serhan,et al. Resolvin E1 and protectin D1 activate inflammation-resolution programmes , 2007, Nature.
[18] C. Serhan. Resolution phase of inflammation: novel endogenous anti-inflammatory and proresolving lipid mediators and pathways. , 2007, Annual review of immunology.
[19] H. Meng,et al. Determinants of host susceptibility in aggressive periodontitis. , 2007, Periodontology 2000.
[20] B. Levy,et al. RvE1 protects from local inflammation and osteoclastmediated bone destruction in periodontitis , 2006, FASEB journal : official publication of the Federation of American Societies for Experimental Biology.
[21] A. Kantarcı,et al. Host-mediated resolution of inflammation in periodontal diseases. , 2006, Periodontology 2000.
[22] J. Beck,et al. Progressive Periodontal Disease and Risk of Very Preterm Delivery , 2006, Obstetrics and gynecology.
[23] C. Serhan. Lipoxins and aspirin-triggered 15-epi-lipoxins are the first lipid mediators of endogenous anti-inflammation and resolution. , 2005, Prostaglandins, leukotrienes, and essential fatty acids.
[24] Shubhada Sankararaman,et al. Cells, tissues and disease: Principles of general pathology , 1997 .
[25] A. Lusis,et al. Arachidonate 5-lipoxygenase promoter genotype, dietary arachidonic acid, and atherosclerosis. , 2004, The New England journal of medicine.
[26] R. Genco,et al. Association of Fcgamma receptor IIa genotype with chronic periodontitis in Caucasians. , 2004, Journal of periodontology.
[27] B. Levy,et al. A Molecular Defect in Intracellular Lipid Signaling in Human Neutrophils in Localized Aggressive Periodontal Tissue Damage1 , 2004, The Journal of Immunology.
[28] M. Marazita,et al. Reevaluation of the chromosome 4q candidate region for early onset periodontitis , 1993, Human Genetics.
[29] J. Ebersole,et al. Rheumatoid factor (RF) distribution in periodontal disease , 1991, Journal of Clinical Immunology.
[30] David M Bohnenkamp,et al. The use of sectional impressions and a transfer index for extensive fixed prosthodontic treatment. , 2004, Compendium of continuing education in dentistry.
[31] Thomas E Van Dyke,et al. Cardiovascular disease and periodontal diseases: commonality and causation. , 2004, Compendium of continuing education in dentistry.
[32] C. Clish,et al. Reduced Inflammation and Tissue Damage in Transgenic Rabbits Overexpressing 15-Lipoxygenase and Endogenous Anti-inflammatory Lipid Mediators 1 , 2003, The Journal of Immunology.
[33] T. Hart,et al. Genes and gene polymorphisms associated with periodontal disease. , 2003, Critical reviews in oral biology and medicine : an official publication of the American Association of Oral Biologists.
[34] C. Serhan,et al. Resolution of Inflammation: A New Paradigm for the Pathogenesis of Periodontal Diseases , 2003, Journal of dental research.
[35] J. Beck,et al. Maternal Periodontal Disease Is Associated With an Increased Risk for Preeclampsia , 2003, Obstetrics and gynecology.
[36] T. Cohnert,et al. Expanding expression of the 5-lipoxygenase pathway within the arterial wall during human atherogenesis , 2003, Proceedings of the National Academy of Sciences of the United States of America.
[37] A. Kantarcı,et al. Neutrophil-mediated tissue injury in periodontal disease pathogenesis: findings from localized aggressive periodontitis. , 2003, Journal of periodontology.
[38] T C Hart,et al. Evaluation of human leukocyte N-formylpeptide receptor (FPR1) SNPs in aggressive periodontitis patients , 2003, Genes and Immunity.
[39] R. Goldberg,et al. Circulating monocyte-platelet aggregates are an early marker of acute myocardial infarction. , 2001, Journal of the American College of Cardiology.
[40] P. Tramini,et al. Serum fatty acid imbalance in bone loss: example with periodontal disease. , 2000, Clinical nutrition.
[41] C. Clish,et al. Lipoxin A(4) analogues inhibit leukocyte recruitment to Porphyromonas gingivalis: a role for cyclooxygenase-2 and lipoxins in periodontal disease. , 2000, Biochemistry.
[42] Parameter on aggressive periodontitis. American Academy of Periodontology. , 2000, Journal of periodontology.
[43] Parameter on Aggressive Periodontitis. , 2000, Journal of periodontology.
[44] T. V. Van Dyke,et al. The acute inflammatory response and the role of phagocytic cells in periodontal health and disease. , 1997, Periodontology 2000.
[45] R. Page,et al. The pathogenesis of human periodontitis: an introduction. , 1997, Periodontology 2000.
[46] S. Offenbacher. Periodontal diseases: pathogenesis. , 1996, Annals of periodontology.
[47] W. Knowler,et al. Severe Periodontitis and Risk for Poor Glycemic Control in Patients with Non-Insulin-Dependent Diabetes Mellitus. , 1996, Journal of periodontology.
[48] S. Pillai,et al. Innate immunity. , 1996, Current opinion in immunology.
[49] T. E. Dyke,et al. TNFα and IL-1β in serum of LJP patients with normal and defective neutrophil chemotaxis , 1994 .
[50] L. Shapira,et al. Priming effect of Porphyromonas gingivalis lipopolysaccharide on superoxide production by neutrophils from healthy and rapidly progressive periodontitis subjects. , 1994, The Journal of Periodontology.
[51] L. Shapira,et al. TNF alpha and IL-1 beta in serum of LJP patients with normal and defective neutrophil chemotaxis. , 1994, Journal of periodontal research.
[52] S. Offenbacher,et al. Changes in crevicular fluid levels of interleukin‐1β, leukotriene B4, prostaglandin E2, thromboxane B2 and tumour necrosis factor α in experimental gingivitis in humans , 1993 .
[53] S. Offenbacher,et al. Changes in crevicular fluid levels of interleukin-1 beta, leukotriene B4, prostaglandin E2, thromboxane B2 and tumour necrosis factor alpha in experimental gingivitis in humans. , 1993, Journal of periodontal research.
[54] S. Offenbacher,et al. Neutrophil surface protein markers as indicators of defective chemotaxis in LJP. , 1990, Journal of periodontology.
[55] C. Serhan,et al. Lipoxin formation during human neutrophil-platelet interactions. Evidence for the transformation of leukotriene A4 by platelet 12-lipoxygenase in vitro. , 1990, The Journal of clinical investigation.
[56] R. Arnold,et al. Neutrophil function in localized juvenile periodontitis. Phagocytosis, superoxide production and specific granule release. , 1986, Journal of periodontology.
[57] M. Hamberg,et al. Lipoxins: novel series of biologically active compounds formed from arachidonic acid in human leukocytes. , 1984, Proceedings of the National Academy of Sciences of the United States of America.
[58] S. Offenbacher,et al. Crevicular fluid prostaglandin E levels as a measure of the periodontal disease status of adult and juvenile periodontitis patients. , 1984, Journal of periodontal research.
[59] F. Dewhirst,et al. Levels of prostaglandin E2, thromboxane, and prostacyclin in periodontal tissues. , 1983, Journal of periodontal research.
[60] S. Socransky,et al. Patterns of progression and regression of advanced destructive periodontal disease. , 1982, Journal of clinical periodontology.
[61] J. Hood. American Academy of Periodontology , 1921 .