The roles of noncoding RNA Rli60 in regulating the virulence of Listeria monocytogenes
The roles of noncoding RNA Rli60 in regulating the virulence of Listeria monocytogenes
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DOI：
10.1016/j.jmii.2014.08.017
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发表时间：
2016-08-01
影响因子：
7.4
通讯作者：
Chen, Chuang-Fu
中科院分区：
文献类型：
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作者：
Peng, Ye-Long;Meng, Qing-Ling;Chen, Chuang-Fu
背景：单增李斯特菌（LM）是一种重要的人畜共患食源性病原体。非编码RNA（ncRNA）在调节其毒力方面发挥着重要作用。然而，作为 ncRNA 的成员，Rli60 在调节 LM 毒力方面的功能仍不清楚。本研究旨在探讨Rli60在调节LM毒力中的作用。方法：采用同源重组方法，构建LM EGD-e rli60基因缺失株（LM-Delta rli60），并与LM EGD-e株在以下方面进行比较：（1）小鼠巨噬细胞系RAW264.7中毒力基因的粘附性、侵袭能力、胞内存活、增殖和毒力基因转录； (2) BALB/c小鼠50%致死剂量(LD50)； (3)小鼠肝脏和脾脏中的含量以及接种后对小鼠肝脏、脾脏和肾脏病理学的影响。结果：与LM EGD-e株相比，LM-Delta rli60株在RAW264.7细胞系中的粘附率显着更高，侵袭率更低，细胞内存活率和增殖率显着更低。接种LM-Delta rli60菌株显着影响毒力基因的转录。 LM-Delta rli60对BALB/c小鼠的LD50增加了2.12个对数级，这表明LM-Delta rli60的毒力显着降低（p < 0.05）。肝脏和脾脏中 LM-Delta rli60 的量显着低于这些器官中 LM EGD-e 的量 (p < 0.05)。 LM-Delta rli60感染对小鼠肝脏、脾脏和肾脏的病理损害低于LM EGD-e感染造成的损害。结论：本研究证实rli60缺失可显着影响LM毒力、粘附、侵袭、存活和增殖。这表明 Rli60 在调节 LM 毒力方面具有重要作用。版权所有(C) 2014，台湾微生物学会。由爱思唯尔台湾有限公司出版。这是一篇遵循 CC BY-NC-ND 许可证 (http://creativecommons.org/licenses/by-nc-nd/4.0/) 的开放获取文章。
Background: Listeria monocytogenes (LM) is an important zoonotic foodborne pathogen. Noncoding RNA (ncRNA) has an important role in regulating its virulence. As a member of ncRNA, however, the function of Rli60 in regulating LM virulence remain unclear. The aim of this study was to investigate the role of Rli60 in regulating LM virulence.Methods: Using a homologous recombination method, a LM EGD-e rli60 gene deletion strain (LM-Delta rli60) was constructed and compared with a LM EGD-e strain in the following respects: (1) adhesiveness, invasion ability, intracellular survival, proliferation, and transcription of virulence genes in the mouse macrophage cell line RAW264.7; (2) 50% lethal dose (LD50) to the BALB/c mouse; and (3) the amount in the mouse liver and spleen and the effects on pathology of mouse liver, spleen, and kidney after inoculation.Results: The LM-Delta rli60 strain had a significantly higher adhesion rate and lower invasion rate with significantly lower intracellular survival and proliferation rates in the RAW264.7 cell line, compared to the LM EGD-e strain. Inoculation with LM-Delta rli60 strain significantly affected the transcription of virulence genes. The LD50 of LM-Delta rli60 to BALB/c mouse was increased by 2.12 logarithmic magnitude, which indicated that the virulence in LM-Delta rli60 is significantly decreased (p < 0.05). The amount of LM-Delta rli60 in the liver and spleen was significantly lower than the amount of LM EGD-e in these organs (p < 0.05). The pathological damage due to LM-Delta rli60 infection in the mouse liver, spleen, and kidney was lower than the damage due to LM EGD-e infection.Conclusion: This study confirmed that the rli60 deletion could significantly affect LM virulence, adhesion, invasion, survival, and proliferation. This suggests that Rli60 has an important role in regulating LM virulence. Copyright (C) 2014, Taiwan Society of Microbiology. Published by Elsevier Taiwan LLC. This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/).