active suppression of early immune response in tobacco by the human pathogen salmonella typhimurium早期免疫反应的活性抑制烟草的人类病原体鼠伤寒沙门氏菌.pdfVIP
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active suppression of early immune response in tobacco by the human pathogen salmonella typhimurium早期免疫反应的活性抑制烟草的人类病原体鼠伤寒沙门氏菌
Active Suppression of Early Immune Response in
Tobacco by the Human Pathogen Salmonella
Typhimurium
Natali Shirron, Sima Yaron*
Faculty of Biotechnology and Food Engineering, Technion, Israel Institute of Technology, Haifa, Israel
Abstract
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 suppressio
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