Plant Immunity Research Group, RIKEN Center for Sustainable Resource Science, Yokohama, 230-0045, Japan.
Graduate School of Environmental and Life Science, Okayama University, Okayama, 700-8530, Japan.
Nat Commun. 2021 Dec 15;12(1):7303. doi: 10.1038/s41467-021-27489-w.
Nonsteroidal anti-inflammatory drugs (NSAIDs), including salicylic acid (SA), target mammalian cyclooxygenases. In plants, SA is a defense hormone that regulates NON-EXPRESSOR OF PATHOGENESIS RELATED GENES 1 (NPR1), the master transcriptional regulator of immunity-related genes. We identify that the oxicam-type NSAIDs tenoxicam (TNX), meloxicam, and piroxicam, but not other types of NSAIDs, exhibit an inhibitory effect on immunity to bacteria and SA-dependent plant immune response. TNX treatment decreases NPR1 levels, independently from the proposed SA receptors NPR3 and NPR4. Instead, TNX induces oxidation of cytosolic redox status, which is also affected by SA and regulates NPR1 homeostasis. A cysteine labeling assay reveals that cysteine residues in NPR1 can be oxidized in vitro, leading to disulfide-bridged oligomerization of NPR1, but not in vivo regardless of SA or TNX treatment. Therefore, this study indicates that oxicam inhibits NPR1-mediated SA signaling without affecting the redox status of NPR1.
非甾体抗炎药（NSAIDs），包括水杨酸（SA），靶向哺乳动物环氧化酶。在植物中，SA 是一种防御激素，调节非表达病原体相关基因 1（NPR1），即免疫相关基因的主转录调节剂。我们发现，oxicam 型 NSAIDs 替诺昔康（TNX）、美洛昔康和吡罗昔康，但不是其他类型的 NSAIDs，对细菌的免疫和 SA 依赖的植物免疫反应具有抑制作用。TNX 处理会降低 NPR1 水平，这与拟议的 SA 受体 NPR3 和 NPR4 无关。相反，TNX 诱导细胞溶质氧化还原状态的氧化，这也受 SA 调节，并调节 NPR1 的动态平衡。半胱氨酸标记测定显示，NPR1 中的半胱氨酸残基可以在体外被氧化，导致 NPR1 的二硫键桥连寡聚化，但在体内无论是否有 SA 或 TNX 处理都不会发生。因此，这项研究表明，oxicam 抑制了 NPR1 介导的 SA 信号，而不影响 NPR1 的氧化还原状态。
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