Hemolymph-dependent and -independent responses in Drosophila immune tissue
Hemolymph-dependent and -independent responses in Drosophila immune tissue
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DOI：
10.1002/jcb.20123
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发表时间：
2004-07-01
影响因子：
4
通讯作者：
Ip, YT
中科院分区：
文献类型：
--
作者：
Bettencourt, R;Asha, H;Ip, YT
昆虫具有类似于哺乳动物先天免疫反应的抗微生物防御反应。先天免疫系统被设计为识别被称为病原体相关分子模式（PAMP）的微生物的保守组分。宿主受体如何检测PAMP并传递信号以启动免疫应答正在被阐明。使用GFP-背，-Dif，和-Relish报告蛋白在离体测定中，我们证明了果蝇脂肪体，一个主要的免疫组织，具有血淋巴依赖性和非依赖性的反应。微生物制剂如脂磷壁酸（LTA）和肽聚糖（PGN）可以刺激解剖和冲洗的幼虫脂肪体的某些反应。因此，识别的至少某些方面可以发生在脂肪体细胞表面，绕过血淋巴的要求。我们的研究结果还表明，从细菌培养物的上清液可以刺激解剖脂肪体的背核易位，但这种刺激是严格的血淋巴依赖性。各种生化分析表明，刺激血淋巴依赖性核转位的细菌上清液中的因子可能由蛋白质组成。我们进一步表明，Dorsal突变幼虫具有低得多的酚氧化酶活性，与Dorsal在先天免疫中比以前显示的更重要的作用一致。(C)2004 Wiley-Liss，Inc.
Insects possess an antimicrobial defense response that is similar to the mammalian innate immune response. The innate immune system is designed to recognize conserved components of microorganisms called pathogen associated molecular patterns (PAMPs). How host receptors detect PAMPs and transmit the signals to mount the immune response is being elucidated. Using GFP-Dorsal, -Dif, and -Relish reporter proteins in ex vivo assays, we demonstrate that Drosophila fat bodies, a major immune tissue, have both hemolymph-dependent and -independent responses. Microbial preparations such as lipoteichoic acid (LTA) and peptidoglycan (PGN) can stimulate some responses from dissected and rinsed larval fat bodies. Therefore, at least some aspects of recognition can occur on fat body cell surfaces, bypassing the requirement of hemolymph. Our results also show that supernatants from bacterial cultures can stimulate the nuclear translocation of Dorsal in dissected fat bodies, but this stimulation is strictly hemolymph-dependent. Various biochemical assays suggest that the factors from bacterial supernatants that stimulate the hemolymph-dependent nuclear translocation are likely made up of proteins. We further show that Dorsal mutant larvae have much lower phenoloxidase activity, consistent with a more important role of Dorsal in innate immunity than previously shown. (C) 2004 Wiley-Liss, Inc.