Department of Food Science and Biotechnology of Animal Resources, Konkuk University, Seoul 05029, Republic of Korea.
J Microbiol Biotechnol. 2020 Jun 28;30(6):926-929. doi: 10.4014/jmb.2001.01038.
This study aimed to determine the immune-stimulating effects of heat-killed Ln1 (HK-Ln1) through the production of nitric oxide (NO) and pro-inflammatory cytokine achieved by inducing NF-κB and mitogen-activated protein kinase (MAPK)-signaling pathways in macrophages. HK-Ln1 showed higher NO and cytokine production compared t°Control (nonstimulated lipopolysaccharide); in addition, the expression of inducible nitric oxide synthase (iNOS) was induced through HK-Ln1treatment. The phosphorylation of IκB-α and p65 increased following treatment by HK-Ln1, which implicates IκB-α degradation and the translocation of p65 to nucleus. In addition, the phosphorylation of MAPKs, ERK 1/2, JNK, and p38 was induced following HK-Ln1 treatment.
本研究旨在通过诱导巨噬细胞中 NF-κB 和丝裂原活化蛋白激酶 (MAPK) 信号通路，确定热灭活 Ln1（HK-Ln1）产生一氧化氮 (NO) 和促炎细胞因子的免疫刺激作用。与对照（未刺激的脂多糖）相比，HK-Ln1 显示出更高的 NO 和细胞因子产生；此外，诱导型一氧化氮合酶 (iNOS) 的表达通过 HK-Ln1 处理诱导。HK-Ln1 处理后，IκB-α 和 p65 的磷酸化增加，这意味着 IκB-α 降解和 p65 向核内易位。此外，HK-Ln1 处理后还诱导了 MAPKs、ERK1/2、JNK 和 p38 的磷酸化。
