These results suggest that calprotectin release is induced by P-LPS via the CD14-TLR2-NF-kappaB signal pathway in human neutrophils and may be dependent on microtubule and microfilament systems.

These results demonstrate that calprotectin release from monocytes is induced by P-LPS, TNF-alpha, and IL-1beta, which in turn, cause and aggravate periodontal disease.

AbstrakEkosistem mangrove memiliki fungsi ekologis sebagai penyerap dan penyimpan karbon. Mangrove menyerap CO 2 pada saat proses fotosintesis, kemudian mengubahnya menjadi karbohidrat dengan menyimpannya dalam bentuk biomassa pada akar ,pohon, serta daun. Tujuan dari penelitian ini adalah untuk mengetahui total above ground biomass, belowground biomass, simpanan karbon atas, simpanan karbon bawah, dan karbon organik pada sedimen dasar di Hutan Mangrove Perancak, Jembrana, Bali. Sampling dilakukan dengan metodepurposive sampling dengan dasar pertimbangan berupa jenis, kerapatan serta diameter pohon mangrove. Estimasi biomassa digunakan metode tanpa pemanenan dengan mengukur diameter at breast height (DBH, 1.3 m) mangrove. Simpanan karbon diestimasi dari 46% biomasa. Kandungan karbon organik pada sedimen diukur dengan menggunakan metode lost on ignition (LOI). Hasil penelitian menunjukkan total above ground biomass sebesar 187,21 ton/ha, below ground biomass sebesar 125,43 ton/ha, simpanan karbon atas sebesar 86,11 ton/ha, simpanan karbon bawah sebesar 57,69 ton/ha, sedangkan karbon organik sedimen sebesar 359,24 ton/ha.

Calprotectin, a major cytosolic protein of leukocytes, is detected in neutrophils, monocytes/macrophages, and epithelial cells. This protein is known to be a marker for several inflammatory diseases and is detected in inflammatory gingival tissue with periodontal disease. Recently, we found that the calprotectin level in gingival crevicular fluid from periodontitis patients was significantly higher than that of healthy subjects. However, the regulation of calprotectin in periodontal disease is unclear. In the present study, we investigated the effect of lipopolysaccharides of periodontopathic bacteria on calprotectin release from human neutrophils. Neutrophils from healthy donors were treated with lipopolysaccharides from Porphyromonas gingivalis (P-LPS), Actinobacillus actinomycetemcomitans, Prevotella intermedia, Fusobacterium nucleatum, and Escherichia coli. Calprotectin of neutrophil was identified by immunoblotting and calprotectin amount was determined by ELISA. Two subunits (10 and 14 kDa) of calprotectin were observed in the cell and medium fractions from neutrophils. P-LPS increased calprotectin release from seven to 16 times the control level after 30 min and its effect appeared in a dose-dependent manner (10-1000 ng/ml). Lipopolysaccharides from A. actinomycetemcomitans, P. intermedia, F. nucleatum, and E. coli also induced calprotectin release from neutrophils. These results suggest that lipopolysaccharides from periodontopathic bacteria induce calprotectin release from human neutrophils.

These results demonstrate that P-LPS, TNF-alpha, and IL-1beta induce calprotectin production from human monocytes and that this production is associated with the activation of DNA C/EBPalpha binding complex.