Hormonal regulation of the humoral innate immune response in Drosophila melanogaster.

Hormonal regulation of the humoral innate immune response in Drosophila melanogaster.
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DOI:
10.1242/jeb.014878
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发表时间:
2008-08
期刊:
The Journal of experimental biology
影响因子:
--
通讯作者:
Silverman N
Silverman N
中科院分区:
其他
文献类型:
--
作者:
Flatt T;Heyland A;Rus F;Porpiglia E;Sherlock C;Yamamoto R;Garbuzov A;Palli SR;Tatar M;Silverman N

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保幼激素 (JH) 和 20-羟基蜕皮激素 (20E) 是用途广泛的激素,可协调昆虫的发育、生长、繁殖和衰老。 20E 的脉冲提供启动发育和生理转变的关键信号,而 JH 以特定阶段的方式促进或抑制这些信号。先前的证据表明 JH 和 20E 可能调节先天免疫,但这些激素是否以及如何相互作用来调节免疫反应仍不清楚。在这里,我们证明 JH 和 20E 对果蝇抗菌肽 (AMP) 基因的诱导具有拮抗作用。免疫刺激后,S2* 细胞的 20E 预处理促进了 AMP 基因的强烈诱导。另一方面,JH III 及其合成类似物 (JHa) 甲氧普林和吡丙醚强烈干扰这种 20E 依赖性免疫增强作用,尽管这些激素不会抑制其他 20E 诱导的细胞变化。同样,对成年果蝇的体内分析证实,JH 是一种激素免疫抑制剂。 S2* 细胞中蜕皮激素受体异二聚体(EcR 或 Usp)任一伴侣的 RNA 沉默可阻止 20E 诱导的免疫增强。相反,沉默甲氧二烯耐受(Met)(一种候选JH受体)并不会损害JH III和JHa的免疫抑制,表明在这种情况下MET不是必要的JH受体。我们的结果表明,20E 和 JH 在响应免疫挑战的基因表达调节中发挥着重要作用。
Juvenile hormone (JH) and 20-hydroxy-ecdysone (20E) are highly versatile hormones, coordinating development, growth, reproduction, and aging in insects. Pulses of 20E provide key signals for initiating developmental and physiological transitions, while JH promotes or inhibits these signals in a stage-specific manner. Previous evidence suggests that JH and 20E might modulate innate immunity, but whether and how these hormones interact to regulate the immune response remains unclear. Here we show that JH and 20E have antagonistic effects on the induction of antimicrobial peptide (AMP) genes in Drosophila melanogaster. 20E pretreatment of S2* cells promoted the robust induction of AMP genes, following immune stimulation. On the other hand, JH III, and its synthetic analogs (JHa) methoprene and pyriproxyfen, strongly interfered with this 20E-dependent immune potentiation, although these hormones did not inhibit other 20E-induced cellular changes. Similarly, in vivo analyses in adult flies confirmed that JH is a hormonal immuno-suppressor. RNA silencing of either partner of the ecdysone receptor heterodimer (EcR or Usp) in S2* cells prevented the 20E-induced immune potentiation. In contrast, silencing methoprene-tolerant (Met), a candidate JH receptor, did not impair immuno-suppression by JH III and JHa, indicating that in this context MET is not a necessary JH receptor. Our results suggest that 20E and JH play major roles in the regulation of gene expression in response to immune challenge.
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