目的:来自植物乳杆菌的脂磷壁酸(L。plantarum)是加剧牙髓炎症的重要毒力因子。脂磷壁酸在调节炎症到增殖相变中起作用,这对于决定牙髓愈合或坏死的结果是至关重要的。本研究探讨植物乳杆菌对雄性大鼠急性牙髓损伤模型淋巴细胞及转化生长因子β1(TGF-β1)和血管内皮生长因子A(VEGF-A)表达的作用。
方法:使用圆形bur在白鼠上磨牙中创建急性牙髓模型。然后,将牙髓暴露于10µg/ml的植物乳杆菌脂磷壁酸中,并填充有临时填充物。在接下来的24、48和72小时内,每只动物都被斩首,用间接免疫组织化学方法分析牙髓中TGF-β1和VEGF-A的表达,而淋巴细胞使用血氧素-伊红染色进行分析。
结果:植物乳杆菌的脂磷壁酸通过增加暴露48和72h后的淋巴细胞数量来诱导急性牙髓(p<0.05)。同时,在暴露48和72小时后抑制TGF-β1表达(p<0.05),暴露72小时后VEGF-A受到抑制(p<0.05)。
结论:暴露于来自植物乳杆菌的脂磷壁酸显著加速牙髓的炎症反应。然而,这种加速的炎症破坏了增殖阶段,可能会对牙髓造成更广泛的损害。
OBJECTIVE: Lipoteichoic acid from Lactobacillus plantarum (L. plantarum) is a significant virulence factor that exacerbates pulp inflammation. Lipoteichoic acid plays a role in modulating the inflammatory to proliferative phase transition is crucial in determining the outcome of pulp healing or necrosis. This study explores the role of L. plantarum on lymphocytes and the expression of transforming growth factor β1 (TGF-β1) and vascular endothelial growth factor A (VEGF-A) in a male rat model of acute dental pulp injury.
METHODS: The acute dental pulp model was created in the upper molar of Rattus novergicus using a round bur. Then, the dental pulp was exposed to 10 µg/ml of the lipoteichoic acid of L. plantarum and filled with a temporary filling. In the next 24, 48, and 72 h, each animal was decapitated, and the expression of TGF-β1 and VEGF-A in dental pulp was analyzed using indirect immunohistochemistry, while the lymphocytes analyzed using hematoxyline-eosin staining.
RESULTS: Lipoteichoic acid of L. plantarum induced acute dental pulp by increasing the lymphocyte number after 48 and 72 h of exposure (p < 0.05). While, inhibiting TGF-β1 expression after 48 and 72 h of exposure (p < 0.05), and VEGF-A was inhibiting after 72 h of exposure (p < 0.05).
CONCLUSIONS: Exposure to lipoteichoic acid from L. plantarum significantly accelerates the inflammatory response in the dental pulp. However, this accelerated inflammation disrupts the proliferative phase, potentially leading to more extensive damage to the dental pulp.