Li Fengwei, Wang Ke, Zhu Xin, Liu Weina, Wu Yanlin, Lv Dashu, Han Yanjing, Wang Xiangchuan, Cheng Daoquan, Chen Tao, Xu Chen, Sun Xianchao
Chongqing Key Laboratory of Plant Disease Biology, College of Plant Protection, Southwest University, Chongqing 400716, China.
Chongqing Key Laboratory of Plant Disease Biology, College of Plant Protection, Southwest University, Chongqing 400716, China.
Pestic Biochem Physiol. 2025 Sep;213:106476. doi: 10.1016/j.pestbp.2025.106476. Epub 2025 May 25.
Tobacco wildfire disease, caused by Pseudomonas syringae pv. tabaci (P. syringae pv. tabaci), severely affects tobacco yield and quality, causing major economic losses. While chemical pesticides are the primary control method, their overuse leads to resistance, resurgence, and residues. Chloroinconazide (CHI) is a tryptophan-derived analog of alkaloid isolated from Peganum harmala, which has been reported to exhibit potent inhibitory activity on viruses and Phytophthora. However, its effectiveness against bacteria remains unclear. To fill this research gap, this study evaluated the effects of CHI on P. syringae pv. tabaci, the causative agent of tobacco wildfire disease, and preliminarily explored its underlying mechanism of action. The results demonstrated that CHI significantly inhibited the in vitro growth of P. syringae pv. tabaci. Further investigation revealed that 50 μg/mL CHI directly acted on the cellular biomembrane of P. syringae pv. tabaci, leading to nucleic acid leakage and ultimately causing cell death. Additionally, 50 μg/mL of CHI can significantly enhance the activity of superoxide dismutase and peroxidase while inhibiting the activity of catalase (CAT), leading to a sharp increase in intracellular hydrogen peroxide levels and consequently inducing oxidative damage in bacterial cells. Furthermore, in vivo experiments further confirmed that 50 μg/mL CHI could induce resistance in tobacco plants against P. syringae pv. tabaci, providing protective effects. Finally, field trials demonstrated that spraying 50 μg/mL CHI significantly reduced the incidence and disease severity index of tobacco wildfire disease. These findings indicate that CHI exhibits significant potential for controlling P. syringae pv. tabaci-induced tobacco wildfire disease, offering a potential alternative strategy for disease management.
烟草野火病由丁香假单胞菌烟草致病变种（Pseudomonas syringae pv. tabaci）引起，严重影响烟草产量和品质，造成重大经济损失。虽然化学农药是主要的防治方法，但过度使用会导致抗性、害虫再猖獗和残留问题。氯吲唑（CHI）是从骆驼蓬中分离出的一种生物碱的色氨酸衍生类似物，据报道对病毒和疫霉具有强大的抑制活性。然而，其对细菌的有效性尚不清楚。为填补这一研究空白，本研究评估了CHI对烟草野火病病原菌丁香假单胞菌烟草致病变种的影响，并初步探讨了其潜在作用机制。结果表明，CHI显著抑制丁香假单胞菌烟草致病变种的体外生长。进一步研究发现，50μg/mL的CHI直接作用于丁香假单胞菌烟草致病变种的细胞膜，导致核酸泄漏，最终引起细胞死亡。此外，50μg/mL的CHI可显著提高超氧化物歧化酶和过氧化物酶的活性，同时抑制过氧化氢酶（CAT）的活性，导致细胞内过氧化氢水平急剧升高，从而诱导细菌细胞的氧化损伤。此外，体内实验进一步证实，50μg/mL的CHI可诱导烟草植株对丁香假单胞菌烟草致病变种产生抗性，提供保护作用。最后，田间试验表明，喷施50μg/mL的CHI可显著降低烟草野火病的发病率和病情严重程度指数。这些发现表明，CHI在控制丁香假单胞菌烟草致病变种引起的烟草野火病方面具有显著潜力，为病害管理提供了一种潜在的替代策略。
