Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P10145 (IL-8)
 23,849 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Within the in vivo environment human gingival fibroblasts (HGF) may be challenged with bacteria or bacterial products. This interaction may result in the release of cytokines which are directly or indirectly involved in connective tissue and bone catabolism, such as interleukin (IL)-1 beta, IL-6, and IL-8. Our investigation has tested the hypothesis that HGF from Actinobacillus actinomycetemcomitans (Aa)-infected patients with rapidly destructive forms of periodontitis, such as localized juvenile periodontitis (LJP), respond to Aa challenge with an exaggerated secretion of IL-1 beta, IL-6, and IL-8. We have compared the in vitro profiles of these cytokines by Aa-challenged HGF obtained from 2 healthy subjects, 2 Aa-infected, slowly progressing adult periodontitis (AP) patients and 2 LJP patients. HGF were challenged throughout a 48-hour period with formalinized whole bacterial cells, and culture supernatants were analyzed for cytokine content using RIA. No differences were noted in the IL-1 beta secretion levels among the different HGF cultures. Although basal (unchallenged) IL-6 and IL-8 production was similar in all HGF cultures, HGF from the two LJP patients responded to Aa challenge with a more rapid IL-6 and a more pronounced IL-8 secretion than healthy or AP HGF. We also tested the ability of human serum antibodies against Aa to moderate the Aa-elicited HGF cytokine secretion by adding human serum, with normal or elevated antibody content. Both sera appeared to have an upregulating effect on IL-6 and IL-8 secretion. Depletion of 95% of the anti-Aa antibody from serum by absorption did not affect its activity. Based on the response of HGF from two LJP patients, we propose that Aa-induced pathology in LJP may be modulated by stimulation of rapid and/or exaggerated secretion of cytokines with potential catabolic effects, although studies with a larger group of LJP patients are needed to further test this hypothesis. Furthermore, serum antibodies against this microorganism do not appear to have a neutralizing effect in cytokine-eliciting HGF-Aa interactions.
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PMID:Gingival fibroblast cytokine profiles in Actinobacillus actinomycetemcomitans-associated periodontitis. 888 44

Localized juvenile periodontitis (LJP) is an early-onset periodontal disease characterized by progressive bone loss involving the permanent first molar and incisor teeth. Approximately 70% to 75% of LJP patients have impaired neutrophil chemotaxis towards a number of chemoattractants including N-formyl-methionyl-leucyl-phenyl-alanine, complement fragment C5a, leukotriene B4, and interleukin 8 (IL-8). The aim of the present study was to observe the role of IL-8 in the pathogenesis of LJP. Fourteen individuals who were systemically and periodontally healthy and 24 systemically healthy individuals diagnosed with LJP (based on the results of clinical periodontal assessments and radiographic examination) were recruited for this study. Gingival crevicular fluid (GCF) samples were obtained from anterior teeth in each subject before treatment. After evaluation of GCF amount from paper strips, enzyme-linked immunoabsorbent assay was employed to determine the amount of IL-8 in GCF. The amount and concentration of IL-8 measured was 894.5 +/- 435 pg, and 445.3 +/- 468 pg/microl for the experimental group and 747.3 +/- 543 pg and 684.7 +/- 548 pg/microl, for the control group. The correlation among the levels of cytokine and clinical parameters was assessed. It was observed that the concentration of IL-8 demonstrated a negative correlation with gingival index in the LJP group. In addition, no significant correlation was found among the total amount and concentration of IL-8, GCF volume, and clinical parameters in the control group. IL-8 is thought to enhance host defense mechanisms against gram-negative bacteria, thus providing protection against periodontal infections. Our data demonstrate that, when both the total amount and concentration of IL-8 are taken into consideration, no significant difference between LJP and healthy subjects is shown. This may indicate a less active IL-8 production compared with healthy subjects in spite of the dense Gram bacterial stimulation in LJP.
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PMID:The correlation of gingival crevicular fluid interleukin-8 levels and periodontal status in localized juvenile periodontitis. 984 41

We used flow cytometry to analyze the expression of adhesion molecules and the oxidative burst of whole-blood polymorphonuclear neutrophils (PMN) from 26 patients with periodontitis. Three different clinical entities were studied: adult periodontitis (AP), localized juvenile periodontitis (LJP), and rapidly progressive periodontitis (RPP). Unstimulated PMN from the patients showed reduced Lewis x, sialyl-Lewis x, and L-selectin expression relative to those from healthy control subjects. These alterations were present whatever the severity of periodontal disease. However, PMN from RPP patients showed increased basal H2O2 production and decreased L-selectin shedding. These latter impairments, which correlated with increased IL-8 plasma levels, could contribute to initial vascular damage. In addition, decreased IL-8 priming of H2O2 production by PMN from RPP patients could account for a lower bactericidal capacity of PMN, leading to the large number of bacteria in the subgingival region of RPP patients. Soluble L-selectin plasma levels were also decreased in the RPP group, indicating more severe or diffuse endothelial damage. These abnormalities were not found in the patients with less destructive forms of periodontitis (AP and LJP). Porphyromonas gingivalis, a bacterial pathogen known to increase IL-8 production by PMN, was found in the periodontal pockets of RPP patients only. These results show links among PMN abnormalities, the clinical form of periodontitis, and the gingival bacterial flora.
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PMID:Neutrophil dysfunctions, IL-8, and soluble L-selectin plasma levels in rapidly progressive versus adult and localized juvenile periodontitis: variations according to disease severity and microbial flora. 1052 6