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Effect of Porphyromonas gingivalis Lipopolysaccharide, Tumor Necrosis Factor‐α, and Interleukin‐1β on calprotectin release in human monocytes
Author(s) -
Kido Junichi,
Hayashi Noriko,
Kataoka Masatoshi,
Nagata Toshihiko
Publication year - 2003
Publication title -
journal of periodontology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.036
H-Index - 156
eISSN - 1943-3670
pISSN - 0022-3492
DOI - 10.1902/jop.2003.74.12.1719
Subject(s) - calprotectin , porphyromonas gingivalis , tumor necrosis factor alpha , lipopolysaccharide , periodontitis , medicine , interleukin , peripheral blood mononuclear cell , inflammation , monocyte , immunology , flow cytometry , cytokine , chemistry , disease , biochemistry , inflammatory bowel disease , in vitro
Background: Calprotection is a major cytosolic protein of monocytes, granulocytes, and epithelial cells. It is known that calprotectin is released in inflammatory tissues and detected in gingival crevicular fluid (GCF) of periodontitis patients at high levels. The origin of calprotectin in GCF and its regulation in periodontal disease are unknown. In this study, we investigated the distribution of calprotectin in gingiva tissues with inflammation and the induction of calprotectin release from human monocytes by lipopolysaccharide of Porphyromonas gingivalis (P‐LPS), tumor necrosis factor‐α (TNF‐α), or interleukin ‐1β(IL‐1β) Methods: Gingival tissues were obtained from a healthy donor and a periodontitis patient and calprotectin in gingival tissues was examined by immunohistochemical staining. Monocytes were isolated from the peripheral blood of healthy donors and cultured with P‐LPS, TNF‐α for 30 minutes to 4 hours. The content of calprotectin in the cell and medium fractions was determined by enzyme‐linked immunosorbent assay (ELISA) Results: Calprotectin was markedly detected at the epithelial and adjacent connective tissue with many inflammatory cells in the gingival tissue from the periodontitis patient. P‐LPS increased calprotectin release from monocytes to the maximum level after 30 minutes of treatment and its level was elevated to about 2‐ to 3‐fold of the control level in a dose‐dependent manner (1 to 1,000 ng/ml). When the effect of TNF‐α and IL‐Iβ on calprotectin release was investigated, calprotectin release significantly increased to about 2.2‐ and 1.5‐fold that of the control level, respectively. Conclusion: These results demonstrate that calprotectin release from monocytes is induced by P‐LPS, TNF‐α, and IL‐lβ, which in turn, cause and aggravate periodontal disease. J Periodontol 2003;74:1719‐1724 .