interleukin-8 and Periapical-Diseases

interleukin-8 has been researched along with Periapical-Diseases* in 2 studies

Other Studies

2 other study(ies) available for interleukin-8 and Periapical-Diseases

ArticleYear
Inflammatory cytokines in saliva: early signs of metabolic disorders in chronic kidney disease. A controlled cross-sectional study.
    Oral surgery, oral medicine, oral pathology, oral radiology, and endodontics, 2010, Volume: 110, Issue:5

    The aim of this study was to evaluate correlations between levels of cytokines in secreted stimulated saliva in patients with chronic kidney disease (CKD) and hyposalivation.. Seventy patients with clearance <20 mL/min/1.73 m(2) were evaluated; 40 were predialysis, 21 hemodialysis, and 9 peritoneal dialysis, and they were matched with 70 control subjects. Salivary flow rate was measured and submandibular/sublingual saliva collected. Analyses were performed for whole protein content using a protein assay, and levels of tumor necrosis factor (TNF) α, interleukin (IL) 1β, γ-interferon (γ-INF), IL-6, IL-8, IL-10, monocyte chemotactic protein (MCP) 1, and soluble intercellular adhesion molecule (sICAM) 1, by using Luminex technology.. Patients with CKD had lower (P = .03) stimulated salivary secretion rate and higher salivary whole protein concentration (P = .002) than control subjects. Concentrations of IL-8 (P = .03) and MCP-1 (P = .002) were decreased and TNF-α/IL-10 (P = .05) and IL-8/IL10 (P = .03) ratios were decreased in CKD patients. CKD patients with low secretion levels of stimulated saliva expressed decreased levels of TNF-α (P = .04), IL-1β (P = .02), γ-INF (P = .03), IL-6 (P = .003), IL-8 (P = .005), MCP-1 (P = .006), and sICAM-1 (P = .02).. Salivary cytokines and secretion rates are significantly decreased in CKD patients. Further research is necessary to understand operating mechanisms and clinical implications of the down-regulation of inflammatory markers in saliva.

    Topics: Case-Control Studies; Chemokine CCL2; Cross-Sectional Studies; Cytokines; Dental Caries; Female; Humans; Inflammation Mediators; Intercellular Adhesion Molecule-1; Interferon-gamma; Interleukin-10; Interleukin-1beta; Interleukin-6; Interleukin-8; Male; Middle Aged; Periapical Diseases; Periodontitis; Peritoneal Dialysis; Renal Dialysis; Renal Insufficiency, Chronic; Saliva; Salivary Proteins and Peptides; Secretory Rate; Sublingual Gland; Submandibular Gland; Tumor Necrosis Factor-alpha; Xerostomia

2010
Interleukin-17 plays a role in exacerbation of inflammation within chronic periapical lesions.
    European journal of oral sciences, 2007, Volume: 115, Issue:4

    Interleukin (IL)-17 plays an important role in inflammation and certain autoimmune diseases. However, its role in the pathogenesis of chronic dental periapical lesions has not been studied. Periapical lesion mononuclear cells (PL-MNC) were isolated from inflammatory cells and phenotypically analyzed by immunocytochemistry. The cells were cultured in vitro and IL-17 and IL-8 were measured in the culture supernatants. Controls were peripheral blood (PB) MNC. The level of IL-17 and the proportion of neutrophils were significantly higher in symptomatic lesions. In addition, the production of IL-17 was higher in culture supernatants of PL-MNC isolated from lesions with a predominance of T cells, and the IL-17 concentration correlated with the proportion of CD3+ and CD4+ cells. There was a positive correlation between the levels of IL-17 and IL-8 in the group of symptomatic lesions. The relationship between these cytokines was additionally confirmed on the basis of augmented production of IL-8 by both PL-MNC and PB-MNC treated with IL-17. Our results suggest that IL-17, by stimulating the production of IL-8, may play a role in exacerbating inflammation within chronic periapical lesions.

    Topics: Adolescent; Adult; Analysis of Variance; Antibodies, Monoclonal; Humans; Immunohistochemistry; Interleukin-17; Interleukin-8; Middle Aged; Monocytes; Periapical Diseases; Periapical Periodontitis; Phenotype; Radiography; Statistics, Nonparametric

2007