Faculty of Biotechnology and Food Engineering, Technion, Israel Institute of Technology, Haifa, Israel.
PLoS One. 2011 Apr 26;6(4):e18855. doi: 10.1371/journal.pone.0018855.
The persistence of enteric pathogens on plants has been studied extensively, mainly due to the potential hazard of human pathogens such as Salmonella enterica being able to invade and survive in/on plants. Factors involved in the interactions between enteric bacteria and plants have been identified and consequently it was hypothesized that plants may be vectors or alternative hosts for enteric pathogens. To survive, endophytic bacteria have to escape the plant immune systems, which function at different levels through the plant-bacteria interactions. To understand how S. enterica survives endophyticaly we conducted a detailed analysis on its ability to elicit or evade the plant immune response. The models of this study were Nicotiana tabacum plants and cells suspension exposed to S. enterica serovar Typhimurium. The plant immune response was analyzed by looking at tissue damage and by testing oxidative burst and pH changes. It was found that S. Typhimurium did not promote disease symptoms in the contaminated plants. Live S. Typhimurium did not trigger the production of an oxidative burst and pH changes by the plant cells, while heat killed or chloramphenicol treated S. Typhimurium and purified LPS of Salmonella were significant elicitors, indicating that S. Typhimurium actively suppress the plant response. By looking at the plant response to mutants defective in virulence factors we showed that the suppression depends on secreted factors. Deletion of invA reduced the ability of S. Typhimurium to suppress oxidative burst and pH changes, indicating that a functional SPI1 TTSS is required for the suppression. This study demonstrates that plant colonization by S. Typhimurium is indeed an active process. S. Typhimurium utilizes adaptive strategies of altering innate plant perception systems to improve its fitness in the plant habitat. All together these results suggest a complex mechanism for perception of S. Typhimurium by plants.
肠病原体在植物上的持久性已经得到了广泛的研究，主要是因为人类病原体如沙门氏菌能够侵入和在植物中生存的潜在危险。已经确定了肠细菌与植物相互作用涉及的因素，因此有人假设植物可能是肠病原体的载体或替代宿主。为了生存，内生细菌必须逃避植物免疫系统，该系统通过植物-细菌相互作用在不同水平上发挥作用。为了了解沙门氏菌如何在植物内生环境中生存，我们对其引发或逃避植物免疫反应的能力进行了详细分析。本研究的模型是暴露于鼠伤寒沙门氏菌血清型 Typhimurium 的烟草植物和细胞悬浮液。通过观察组织损伤以及测试氧化爆发和 pH 值变化来分析植物免疫反应。结果发现，污染植物中的鼠伤寒沙门氏菌并未促进疾病症状的发生。活鼠伤寒沙门氏菌不会引发植物细胞产生氧化爆发和 pH 值变化，而热致死或氯霉素处理的鼠伤寒沙门氏菌和纯化的沙门氏菌脂多糖则是显著的诱导剂，表明鼠伤寒沙门氏菌积极抑制植物反应。通过观察植物对缺失毒力因子的突变体的反应，我们表明这种抑制依赖于分泌因子。缺失 invA 降低了鼠伤寒沙门氏菌抑制氧化爆发和 pH 值变化的能力，表明功能性 SPI1 TTSS 是抑制所必需的。本研究表明，鼠伤寒沙门氏菌对植物的定殖确实是一个主动过程。鼠伤寒沙门氏菌利用改变固有植物感知系统的适应性策略来提高其在植物栖息地中的适应性。所有这些结果表明，植物对鼠伤寒沙门氏菌的感知存在一种复杂的机制。
