Sosroseno W, Musa M, Ravichandran M, Fikri Ibrahim M, Bird P S, Seymour G J
Department of Oral Biology, School of Dental Sciences, University Sains Malaysia, Kota Bharu, Malaysia.
Oral Microbiol Immunol. 2006 Jun;21(3):145-50. doi: 10.1111/j.1399-302X.2006.00262.x.
The aim of the present study was to determine whether or not lipopolysaccharide from Actinobacillus actinomycetemcomitans could stimulate arginase activity in a murine macrophage cell line (RAW264.7 cells).
RAW264.7 cells were treated with A. actinomycetemcomitans-lipopolysaccharide or lipopolysaccharide from Escherichia coli for 24 h. The effect of polymyxin B, l-norvaline, dl-norvaline, dexamethasone and cytokines (interferon-gamma and interleukin-4) on arginase activity in A. actinomycetemcomitans-lipopolysaccharide-stimulated cells was also determined. The cells were pretreated with anti-CD14, anti -toll-like receptor 2, or anti-toll-like receptor 4 antibody prior to stimulation with A. actinomycetemcomitans-lipopolysaccharide. Arginase activity was determined by a colorimetric assay.
A. actinomycetemcomitans-lipopolysaccharide stimulated arginase activity in RAW264.7 cells in a dose-dependent manner, but was less potent than E. coli-lipopolysaccharide. Polymyxin B and l-norvaline, but not dl-norvaline, blocked the arginase activity in A. actinomycetemcomitans-lipopolysaccharide-stimulated cells. Dexamethasone and interleukin-4 but not interferon-gamma augmented arginase activity in A. actinomycetemcomitans-lipopolysaccharide-stimulated cells. Treatment of the cells with anti-CD14 and anti-toll-like receptor 4 but not anti-toll-like receptor 2 antibody decreased arginase activity in A. actinomycetemcomitans-lipopolysaccharide-stimulated cells.
The results of the present study suggest that lipopolysaccharide from A. actinomycetemcomitans via CD14/toll-like receptor 4 complex molecules and the regulatory control of glucocorticoid and cytokines may stimulate arginase activity in RAW264.7 cells.
本研究旨在确定伴放线放线杆菌的脂多糖是否能刺激小鼠巨噬细胞系（RAW264.7细胞）中的精氨酸酶活性。
用伴放线放线杆菌脂多糖或大肠杆菌脂多糖处理RAW264.7细胞24小时。还测定了多粘菌素B、L-正缬氨酸、DL-正缬氨酸、地塞米松和细胞因子（γ干扰素和白细胞介素-4）对伴放线放线杆菌脂多糖刺激细胞中精氨酸酶活性的影响。在用伴放线放线杆菌脂多糖刺激之前，先用抗CD14、抗Toll样受体2或抗Toll样受体4抗体对细胞进行预处理。通过比色法测定精氨酸酶活性。
伴放线放线杆菌脂多糖以剂量依赖性方式刺激RAW264.7细胞中的精氨酸酶活性，但效力低于大肠杆菌脂多糖。多粘菌素B和L-正缬氨酸而非DL-正缬氨酸可阻断伴放线放线杆菌脂多糖刺激细胞中的精氨酸酶活性。地塞米松和白细胞介素-4而非γ干扰素可增强伴放线放线杆菌脂多糖刺激细胞中的精氨酸酶活性。用抗CD14和抗Toll样受体4而非抗Toll样受体2抗体处理细胞可降低伴放线放线杆菌脂多糖刺激细胞中的精氨酸酶活性。
本研究结果表明，伴放线放线杆菌的脂多糖可能通过CD14/Toll样受体4复合分子以及糖皮质激素和细胞因子的调节控制来刺激RAW264.7细胞中的精氨酸酶活性。
