Expression of monocyte chemoattractant protein 1 (MCP-1) in adult periodontal disease: increased monocyte chemotactic activity in crevicular fluids and induction of MCP-1 expression in gingival tissues

Abstract

The present study shows that monocyte chemotactic activity in crevicular fluids increases with severity of the disease and that a monocyte chemoattractant, monocyte chemoattractant protein 1 (MCP-1), is expressed as the predominant cytokine of gingival tissues and their fibroblasts treated with Porphyromonas (Bacteroides) gingivalis lipopolysaccharide (P-LPS). High monocyte chemotactic activity in the crevicular fluids was neutralized significantly by antiserum specific for the JE/MCP-1 protein. Marked expression of the MCP-1 gene was observed in the gingival tissues of all adult periodontal patients tested, but not in those of healthy subjects. Monocyte chemotactic activity was observed in culture supernatants of human normal gingival tissues treated with P-LPS, and the chemotactic activity increased in a dose-related manner. Expression of MCP-1 in P-LPS-treated human gingival fibroblasts was further examined. P-LPS induced the MCP-1 gene expression in a dose-and treatment time-dependent manner. The MCP-1 gene product in the culture supernatant was detected as two forms with molecular masses of 11,000 and 15,000 Da by immunoprecipitation with the specific antiserum. The MCP-1 gene expression was induced in the fibroblasts treated with interleukin-113 and tumor * Corresponding author. apparently unique property since other characterized chemoattractants such as leukotriene B4, platelet-activating factor, and C. are not specific for monocytes.

Gingival Crevicular Fluid Levels of Monocyte Chemoattractant Protein‐1 and Tumor Necrosis Factor‐Alpha in Patients With Chronic and Aggressive Periodontitis

“…As MCP-1 expression is important to chemotaxis of the monocytes, the detection of GCF MCP-1 levels, especially in AgP, might clarify whether the MCP-1 expression pattern is different from chronic periodontal diseases. In a previous study, Hanazawa et al 20 examined MCP-1 gene expression in gingival tissues and monocyte chemotactic activity in GCF from the patients with periodontal diseases. In the findings of their study, marked MCP-1 gene expression was demonstrated in gingival tissues from chronic periodontal patients but not in those from healthy subjects.…”

“…However, the immunopathogenic mechanisms in the aggressive form of periodontal diseases have not been completely elucidated. Although the expression of MCP-1 in gingival tissue samples with chronic periodontal disease and chemotactic activity of monocytes in gingival crevicular fluid (GCF) have been investigated in previous studies, 20,21 to our knowledge there is not any report examining and comparing the levels of MCP-1 in GCF samples obtained from patients with chronic periodontitis (CP) and AgP. The investigation of MCP-1 levels in GCF and the relationship between GCF levels of MCP-1 and TNF-a seem very important for further understanding the functional role of MCP-1 and TNF-a in chronic and aggressive periodontal diseases.…”

Mechanisms ofPorphyromonas gingivalis-induced monocyte chemoattractant protein-1 expression in endothelial cells

“…Monocyte chemoattractant protein-1 (MCP-1), a C-C chemokine, is one of the most potent chemoattractants for monocytes and activation of monocytes by endothelium-derived MCP-1 may be an essential step in the cascade of events that ultimately leads to the emigration of monocytes into inflamed tissue [6]. Fibroblasts, mononuclear phagocytes, and endothelial cells express MCP-1 in inflamed gingiva [7], and MCP-1 increases in the crevicular fluids of adult periodontal patients with severity of the disease [8]. Therefore, MCP-1 production by bacterially stimulated gingival endothelial cells should contribute to periodontal disease progression.…”

Interleukin-6 negatively regulatesPorphyromonas gingivalisfimbria-stimulated fibronectin expression in human gingival fibroblasts

“…rial pathogenesis depends on the production of endogenous IL-6 by periodontal tissues stimulated by the fimbriae. As we previously demonstrated, the fimbriae contribute to the inflammation and alveolar bone loss of periodontal tissues that occurs in chronic periodontal patients via the multipotential action of endogenous inflammatory cytokines such as IL-1, IL-6, TNF-a, MCP-1, and so on [1][2][3]15]. Therefore, these results suggest to us the possibility that, directly or indirectly, IL-6 plays an important role in the fimbria-mediated pathogenesis in chronic periodontal disease; because IL-6 inhibited the fimbria-stimulated FN expression.…”

“…Chronic periodontal disease has been characterized by gingival tissue inflammation, loss of periodontal ligament, and alveolar bone resorption. We previously demonstrated that the gene for monocyte chemoattractant protein 1 (MCP-1) was markedly expressed in gingival tissues of patients with advanced periodontitis and that monocyte chemotactic activity in the GCF of chronic periodontal patients increased with the severity of the disease [15]. MCP-1 expression was observed in the fimbria-or lipopolysaccharide-treated human gingival fibroblasts.…”