Butyric acid induces apoptosis in both human monocytes and lymphocytes equivalently
Butyric acid induces apoptosis in both human monocytes and lymphocytes equivalently
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DOI：
10.2334/josnusd.54.7
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发表时间：
2012-03-01
影响因子：
1.9
通讯作者：
Abe, Kazumasa
中科院分区：
文献类型：
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作者：
Abe, Kazumasa
短链脂肪酸（SCFAs）是厌氧牙周病细菌的代谢物，可诱导免疫细胞（如淋巴细胞、单核细胞和巨噬细胞）凋亡。然而，目前尚不清楚来自病原体的SCFAs是否会像诱导淋巴细胞一样诱导单核细胞/巨噬细胞凋亡。本研究探讨了scfas诱导的免疫调节细胞凋亡是否相同。用各种牙周病细菌培养上清液或丁酸钠处理后，观察细胞凋亡情况。细胞凋亡和细胞活力分别通过DNA片段检测和MTS检测试剂盒检测。牙龈卟啉单胞菌和核梭杆菌培养滤液强烈诱导THP-1和U937人单核细胞和巨噬细胞凋亡，而黑化普雷沃特菌和普雷沃特菌培养基培养滤液未能诱导凋亡。健康牙龈成纤维细胞和口腔上皮细胞对所有培养滤液均有抗性。气液色谱法在培养滤液中检测到丁酸（21.0 ~ 34.0 mM），而在黑皮假体和中间假体中仅检测到微量丁酸。这些结果表明，由牙周病细菌产生的丁酸以一致的方式严重损害免疫调节细胞，同样可能参与介导牙周慢性炎症。
Short-chain fatty acids (SCFAs) are metabolites from anaerobic periodontopathic bacteria that induce apoptosis in immune cells such as lymphocytes, monocytes and macrophages. However, it remains unclear if SCFAs from pathogens induce apoptosis in monocytes/macrophages similarly with lymphocytes. This study investigated whether SCFAs-induced apoptosis is equal among the immunoregulatory cells. Cell apoptosis of the employed human cells was evaluated after treatment with culture supernatants from various periodontopathic bacteria or sodium butyrate. Apoptosis and viability were determined by detection of DNA fragmentation and using an MTS assay kit, respectively. Porphyromonas gingivalis and Fusobacterium nucleatum culture filtrates strongly induced apoptosis whereas Prevotella nigrescens and Prevotella intermedia culture filtrates failed to induce apoptosis in the THP-1 and U937 human monocyte and macrophage cell lines. Healthy gingival fibroblasts and oral epithelial cells were resistant to all the culture filtrates. Gas-liquid chromatography detected butyric acid in P. gingivalis (21.0-34.0 mM) and F. nucleatum (36.0 mM) in culture filtrates, whereas, only trace levels were seen in P. nigrescens and P. intermedia. These results suggest that butyric acid produced by periodontopathic bacteria severely damages immunoregulatory cells in a consistent manner and, likewise, could be involved in mediating periodontal chronic inflammation.