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A Potential Role of an Intracellular Signaling Defect in Neutrophil Functional Abnormalities and Promotion of Tissue Damage in Patients with Localized Juvenile Periodontitis
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Lasse Leino
Veröffentlicht/Copyright:
1. Juni 2005
Abstract
Localized juvenile periodontitis is a destructive form of periodontal inflammatory disease which has its onset at puberty. The etiopathology of the disease is still unclear but neutrophils have been suggested to play a major role both in the production and development of the disorder. About 70 % of the patients with localized juvenile periodontitis exhibit neutrophil functional abnormalities, such as decreased chemotaxis and phagocytosis. Interestingly, it has been frequently reported that the same hypoactive cells show an enhanced respiratory burst response and increased adhesion. Several possible mechanisms explaining neutrophil anomalies in localized juvenile periodontitis have been proposed. These include the presence of soluble serum factors capable of modulating neutrophil function, altered cell-surface receptor expression and/or function, and a change in the post-receptor signaling events. Recently, a growing evidence has accumulated showing that the diacylglycerol metabolism could be altered in neutrophils from patients with localized juvenile periodontitis. This change, which may be due to a defect in a major diacylglycerol metabolizing enzyme, diacylglycerol kinase, results in enhanced accumulation of diacylglycerol in activated cells. Because diacylglycerol is an endogenous activator of protein kinase C, the increased and prolonged generation of diacylglycerol could lead to abnormal pattern of protein kinase C-regulated neutrophil functions, explaining the parallel hypo- and hyperactivities.
:
Published Online: 2005-06-01
Published in Print: 1999-03-01
Copyright (c)1999 by Walter de Gruyter GmbH & Co. KG
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Artikel in diesem Heft
- IFCC/Beckman European Conference 1998 Frontiers in Molecular Basis of Disease: Inflammatory Diseases
- Frontiers in Molecular Basis of Disease: Inflammatory Diseases
- Mechanisms of Antigen Presentation
- How to Extinguish Lymphocyte Activation, Immunotyrosine-Based Inhibition Motif (ITIM)-Bearing Molecules a Solution?
- Association between Reduced Human Leukocyte Antigen (HLA)-DR Expression on Blood Monocytes and Increased Plasma Level of Interleukin-10 in Patients with Severe Burns
- Immunostimulatory CpG Motifs Trigger a T Helper-1 Immune Response to Human Immunodeficiency Virus Type-1 (HIV-1) gp160 Envelope Proteins
- Activation and Regulation of NFκB during Acute Inflammation
- CD 14++ Monocytes, CD14+/CD16+ Subset and Soluble CD14 as Biological Markers of Inflammatory Systemic Diseases and Monitoring Immuno-suppressive Therapy
- A Potential Role of an Intracellular Signaling Defect in Neutrophil Functional Abnormalities and Promotion of Tissue Damage in Patients with Localized Juvenile Periodontitis
- Polymorphonuclear Oxidative Burst after Helicobacter pylori Water Extract Stimulation Is not Influenced by the Cytotoxic Genotype but Indicates Infection and Gastritis Grade
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