| 摘要: |
| ［摘要］ 目的 探讨瘦素抑制巨噬细胞中马尔尼菲篮状菌（TM）增殖的机制。方法 培养THP-1细胞并经佛波酯（PMA）刺激诱导分化为THP-1巨噬细胞，加入TM共培养，洗去未被吞噬的TM孢子。实验组予瘦素进行干预，对照组不予瘦素干预。应用菌落形成单位（CFU）实验检测THP-1巨噬细胞中TM的增殖情况。应用实时荧光定量PCR法检测Toll样受体（TLRs）及其下游信号通路因子的mRNA表达水平。结果 CFU实验结果显示，终浓度为1～15 μg/ml瘦素均可有效抑制THP-1巨噬细胞中TM的增殖（P<0.05），且在终浓度为5 μg/ml时即可获得最佳的抑制效应。实时荧光定量PCR结果显示，实验组TLR2、TLR6 mRNA表达水平高于对照组，差异有统计学意义（P<0.05），但两组TLR3、TLR4、TLR7 mRNA表达水平比较差异无统计学意义（P>0.05）。实验组髓样分化原发反应基因88（MyD88）、促分裂原活化蛋白激酶1（MAPK1）、白介素（IL）-1β mRNA表达水平高于对照组，IL-6 mRNA表达水平低于对照组，差异有统计学意义（P<0.05），但两组肿瘤坏死因子（TNF）-α和巨噬细胞炎症蛋白1α（MIP-1α） mRNA表达水平比较差异无统计学意义（P>0.05）。结论 瘦素可以抑制THP-1巨噬细胞中TM的增殖，这可能是通过上调TLR2/6信号通路、激活炎症因子实现的。 |
| 关键词: 瘦素 马尔尼菲篮状菌 Toll样受体 炎症因子 |
| DOI：10.3969/j.issn.1674-3806.2021.12.05 |
| 分类号:R 392.1 |
| 基金项目:国家自然科学基金项目（编号：81971934）；广西自然科学基金“杰出青年”项目（编号：2018GXNSFFA281001） |
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| A study on the mechanism of leptin inhibiting proliferation of Talaromyces marneffei in macrophages |
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WEN Liu-fang, TANG Qiao, WANG Xin-wei, et al.
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School of Public Health, Guangxi Medical University, Guangxi Key Laboratory of Acquired Immune Deficiency Syndrome Prevention and Treatment, Nanning 530021, China
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| Abstract: |
| ［Abstract］ Objective To explore the mechanism of leptin inhibiting proliferation of Talaromyces marneffei(TM) in macrophages. Methods THP-1 cells were cultured and induced to differentiate into THP-1 macrophages by stimulation of phorbol 12-myristate 13-acetate(PMA), and TM was add for co-culture, and the unswallowed TM spores were washed away. The experimental group was treated with leptin, and the control group was not treated with leptin. The colony forming unit(CFU) experiment was used to detect the proliferation of TM in THP-1 macrophages. Real-time fluorescent quantitative polymerase chain reaction(PCR) was used to detect the mRNA expression levels of Toll-like receptors(TLRs) and its downstream signal pathway factors. Results The results of CFU experiment showed that leptin could effectively inhibit the proliferation of TM in THP-1 macrophages at a final concentration of 1-15 μg/ml(P<0.05), and the best inhibition effect could be obtained at a final concentration of 5 μg/ml. The results of real-time fluorescent quantitative PCR showed that the expression levels of TLR2 and TLR6 mRNA in the experimental group were higher than those in the control group, and the differences were statistically significant(P<0.05), but there were no significant differences in the expression levels of TLR3, TLR4, and TLR7 mRNA between the two groups(P>0.05). The expression levels of myeloid differentiation factor 88(MyD88), mitogen-activated protein kinase 1(MAPK1), interleukin-1β(IL-1β) mRNA in the experimental group were higher than those in the control group, and the expression level of IL-6 mRNA in the experimental group was lower than that in the control group, and the differences were statistically significant(P<0.05), but there were no significant differences in the expression levels of tumor necrosis factor α(TNF-α) and macrophage inflammatory protein 1α(MIP-1α) mRNA between the two groups(P>0.05). Conclusion Leptin can inhibit the proliferation of TM in THP-1 macrophages, which may be achieved by up-regulating the TLR2/6 signaling pathway and activating inflammatory factors. |
| Key words: Leptin Talaromyces marneffei(TM) Toll-like receptors(TLRs) Inflammatory factors |
