National "111" Center for Cellular Regulation and Molecular Pharmaceutics, Key Laboratory of Fermentation Engineering (Ministry of Education), School of Food and Biological Engineering, Hubei University of Technology, Hubei, China.
Guelph Research and Development Centre, Agriculture and Agri-Food Canada, Guelph, ON, Canada.
Front Immunol. 2021 Mar 8;12:653205. doi: 10.3389/fimmu.2021.653205. eCollection 2021.
DT104 infection causes the death of , which can be prevented by certain isolates. However, the molecular mechanisms of both the host response to the infection and the protection by are largely unclear. The present study has investigated the life-span and gene expression of both wild-type (WT) and mutants in some key components of cell signaling in response to infection and protection from . The results indicated that the gene expression of in the DAF/ insulin-like growth factor (DAF/IGF) pathway, and in the programmed cell death (PCD) pathway, , and for antimicrobial peptide production, and involved in the production of other defense molecules was all significantly upregulated when the wild-type (WT) was subjected to DT104 infection. On the contrary, the gene expression of , and in the p38 mitogen-activated protein kinase (MAPK) pathway and , and for the production of other defense molecules was significantly suppressed by DT104. Pretreatment of the worms with LB1 significantly upregulated the expression of almost all the tested genes except for , and compared with the nematode infected with DT104 only. Mutants defective in the cell signaling or other defense molecules of were either more susceptible (defective in , or ) or more resistant (defective in or ) to DT104 infection than the WT except for the mutant defective in . Mutants defective in antimicrobial peptides ( or ) were also more susceptible than the WT. In contrast, the mutant defective in became more resistant. When all the mutants were pretreated with LB1, five mutants that are defective in , or showed no response to the protection from LB1. These results suggest that LB1 can regulate cell signaling including the p38 MAPK pathway and downstream production of antimicrobial peptides and defense molecules to combat infection.
DT104 感染导致死亡，某些可以预防。然而，宿主对感染的反应和保护的分子机制在很大程度上尚不清楚。本研究调查了野生型（WT）和某些细胞信号关键成分突变体在感染 DT104 后的寿命和基因表达以及对的保护作用。结果表明，DAF/胰岛素样生长因子（DAF/IGF）途径中的基因表达、程序性细胞死亡（PCD）途径中的、和抗菌肽的产生，以及参与其他防御分子产生的都被显著上调。当野生型（WT）受到 DT104 感染时。相反，p38 丝裂原活化蛋白激酶（MAPK）途径中的和和其他防御分子的产生，以及的基因表达被 DT104 显著抑制。用 LB1 预处理线虫可显著上调除和以外的几乎所有检测基因的表达。与仅感染 DT104 的线虫相比，信号转导或其他防御分子缺陷的突变体对 DT104 感染的敏感性更高（缺陷或）或更耐药（缺陷或），除缺陷外。抗菌肽缺陷（或）的突变体也比野生型更敏感。相反，缺陷的突变体变得更耐药。当所有突变体都用 LB1 预处理时，五个缺陷或或的突变体对 LB1 的保护没有反应。这些结果表明，LB1 可以调节包括 p38 MAPK 途径在内的细胞信号转导以及抗菌肽和防御分子的下游产生，以抵抗 DT104 感染。
