Interleukin-8 is a major neutrophil chemotactic factor derived from cultured human gingival fibroblasts stimulated with interleukin-1 beta or tumor necrosis factor alpha

Abstract

Inflammatory mediators produced by cells in the gingiva have been implicated in the initiation and progression of periodontal disease, a common infectious disease. In this study, we examined the biological activity of neutrophil chemotactic factors and the kinetics of expression of interleukin-8 (IL-8) mRNA derived from normal gingival fibroblasts in response to inflammatory mediators in an in vitro model. Gingival fibroblasts stimulated by either recombinant human interleukin-1 beta or recombinant human tumor necrosis factor alpha produced neutrophil chemotactic factors after 4 h, whereas expression of cell-derived IL-8 mRNA was detected within 1 h after stimulation. Furthermore, in a neutralization assay, rabbit anti-recombinant human IL-8 antiserum inhibited neutrophil chemotactic activity to basal levels. These results provide evidence that gingival fibroblasts synthesize potent chemotactic factors such as IL-8 in the presence of the inflammatory mediators interleukin-1 beta and tumor necrosis factor alpha. The activity of these factors may contribute to neutrophil-mediated processes in the pathogenesis of periodontal disease.

Megakaryocytes derived from CD34‐positive cord blood cells produce interleukin‐8

“…These results are consistent with the evidence that IL-1b and IL-6 mRNA synthesis in monocytes requires stimulation with lipopolysaccharides (LPS), but IL-8 mRNA is expressed in the absence of LPS, as described by de Waal Malefyt et al (1991). However, in contrast to monocytes-macrophages and fibroblasts (De et al, 1995;Kristensen et al, 1991;Takashiba et al, 1992), megakaryocytes responded to neither IL-1a nor TNF-a alone. The combination of TPO with IL-1a, but not TNF-a, is necessary to enhance IL-8 secretion from megakaryocytes.…”

Porphyromonas gingivalisfimbriae and their synthetic peptides induce proinflammatory cytokines in human peripheral blood monocyte cultures

“…In this regard, IL-1/3 has been shown to induce bone resorption [21]. They also stimulated osteoblastic cells to induce another cytokine gene [22], which in turn induced IL-8 production in gingival fibroblast cultures [23]. These findings suggest that inflammatory ceils produce various cytokines in response to microbial stimulants including P. gingivalis fimbriae and the cytokine network may contribute to progression of tissue destruction in periodontal diseases.…”

Analysis of Interleukin‐Activated Human Gingival Fibroblasts: Modulation of Chemokine Responses by Female Hormones

“…Such an autocrine effect also could modify the tissue microenvironment in a manner that contributes to the pathogenesis of periodontal disease. 3 Another potential autocrine/paracrine system which apparently was stimulated in this in vitro model involves the endothelin (ET), endothelin receptor pair ( Table 1). Gene expression for each of these proteins was upregulated in GF more than 2-fold by IL-1β.…”