Enteric bacteria counteract lipopolysaccharide induction of antimicrobial peptide genes
Enteric bacteria counteract lipopolysaccharide induction of antimicrobial peptide genes
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DOI：
10.4049/jimmunol.167.12.6920
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发表时间：
2001-12-15
影响因子：
4.4
通讯作者：
Söderhäll, K
中科院分区：
文献类型：
--
作者：
Lindmark, H;Johansson, KC;Söderhäll, K
果蝇的体液免疫涉及抗菌肽的产生，这是由进化保守的微生物分子（如脂多糖）诱导的。通过使用果蝇 mbn-2 细胞，我们发现活细菌，包括大肠杆菌、鼠伤寒沙门氏菌、胡萝卜软腐欧文氏菌和铜绿假单胞菌，可以阻止 LPS 诱导抗菌肽基因，而藤黄微球菌和马链球菌则不能。在每个 mbn-2 细胞 20 个细菌水平上观察到抑制作用，而在不添加 LPS 的情况下，抗菌肽也在较低的细菌浓度（每个细胞少于或等于 2 个细菌）下被诱导。凝胶转移实验表明，抑制作用位于转录因子 Relish（NF-kappaB/Rel 家族成员）的上游或激活水平。细菌必须与细胞有物理接触，但不能被吞噬，以防止 LPS 诱导。有趣的是，至少对于大肠杆菌来说，抑制机制独立于 III 型分泌系统，这表明该抑制机制与之前描述的耶尔森氏菌 YopJ 的抑制机制无关。
The humoral immunity of Drosophila involves the production of antimicrobial peptides, which are induced by evolutionary conserved microbial molecules, like LPS. By using Drosophila mbn-2 cells, we found that live bacteria, including E. coli, Salmonella typhimurium, Erwinia carotovora, and Pseudomonas aeruginosa, prevented LPS from inducing antimicrobial peptide genes, while Micrococcus luteus and Streptococcus equi did not. The inhibitory effect was seen at bacterial levels from 20 per mbn-2 cell, while antimicrobial peptides were induced at lower bacterial concentrations (less than or equal to2 bacteria per cell) also in the absence of added LPS. Gel shift experiment suggests that the inhibitory effect is upstream or at the level of the activation of the transcription factor Relish, a member of the NF-kappaB/Rel family. The bacteria have to be in physical contact with the cells, but not phagocytosed, to prevent LPS induction. Interestingly, the inhibiting mechanism is, at least for E. coli, independent of the type III secretion system, indicating that the inhibitory mechanism is unrelated to the one earlier described for YopJ from Yersinia.