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Perception of a quorum sensing signal by cell surface immune receptors increases plant disease resistance

ABSTRACT: Bacterial quorum sensing (QS) during pathogenesis is an indicator of increasing danger. How sessile plants perceive QS for defense is unclear. Here, we show that Arabidopsis thaliana perceives 2'-aminoacetophenone (2’-AA), a volatile QS signal from Pseudomonas aeruginosa, through cell surface pattern recognition receptor (PRR) complexes, resulting in multistrategic defense and disease resistance. The 2’-AA-induced plant immunity requires chemical and genetic specificity. 2’-AA binds to the cytoplasmic domain of BRI1-ASSOCIATED RECEPTOR KINASE1 (BAK1) and induces the formation of PRR complexes that initiate the plant immune responses. 2’-AA stimulates plant exudation of acetic acid, a volatile compound that effectively quenches QS and inhibits P. aeruginosa virulence. Plants exposed to 2’-AA reshaped the root microbiome by suppressing the abundant Pseudomonad taxa with increased bacterial diversity. These results illustrate the ability of plants to perceive and respond to pathogen QS.

ORGANISM(S): Pseudomonas aeruginosa

PROVIDER: GSE270548 | GEO | 2026/04/16

REPOSITORIES: GEO

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Project description:Pseudomonas aeruginosa (PA) causes severe respiratory infections utilizing multiple virulence functions. Our previous findings on PA quorum sensing (QS)-regulated small molecule, 2’-aminoacetophenone (2-AA), secreted in host infected tissues, revealed its effect on immune and metabolic functions favoring a long-term presence of PA in host tissues. However, studies on 2-AA’s effect on bronchial-airway epithelium and pulmonary endothelium remain elusive. To evaluate 2AA’s spatiotemporal changes in the human airway, considering endothelial cells as the first point of contact when the route of lung infection is through the bloodstream, we utilized the microfluidic bronchial-airway-on-a-chip lined by polarized human bronchial-airway epithelium and pulmonary endothelium. Using this platform, we performed RNA-sequencing to analyse responses of 2-AA treated primary human pulmonary microvascular endothelium (HPMEC) and adjacent primary normal human bronchial epithelial (NHBE) cells from healthy female donors and potential cross-talk between these cells. Analyses unveiled specific signaling and biosynthetic pathways to be differentially regulated by 2-AA in epithelial cells, including HIF-1 and pyrimidine signaling, glycosaminoglycan, and glycosphingolipid biosynthesis, while in endothelial cells were fatty acid metabolism, phosphatidylinositol and estrogen receptor signaling, and the proinflammatory signaling pathways. As part of the significant overlap in gene regulation and signaling pathways in both cell types impacted by 2-AA were genes implicated in immune response and cellular functionality. Moreover, we found cellular responses differentially regulated in each cell type, affecting barrier permeability, cholesterol metabolism, and oxidative phosphorylation. These 2-AA-mediated distinct responses may result from the cross-talk between these cells. Murine in-vivo and additional in vitro cell culture studies confirmed cholesterol accumulation and its effect on lung physiology by 2-AA. Results also revealed specific biomarkers associated with cystic fibrosis and idiopathic pulmonary fibrosis to be modulated by 2-AA in both cell types, with the cystic fibrosis transmembrane regulator expression to be affected only in endothelial cells. The 2-AA-mediated effects on epithelial and endothelial cells within a microphysiological dynamic environment that mimics the human lung airway enhance our understanding of the influence of this QS signaling molecule in HPMEC and NHBE cells. This study provides novel insights into their functions and potential interactions, paving the way for innovative therapeutic strategies to combat PA lung infections.

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Perception of a quorum sensing signal by cell surface immune receptors increases plant disease resistance

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