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Nicotinamide adenine dinucleotide (NAD) is a pivotal coenzyme that has emerged as a central hub linking redox equilibrium and signal transduction in living cells. The homeostasis of NAD is required for plant growth, development, and adaption to environmental stresses. Quinolinate phosphoribosyltransferase (QPRT) is a key enzyme in NAD de novo synthesis pathway. T-DNA-based disruption of <i>QPRT</i> gene is embryo lethal in <i>Arabidopsis thaliana</i>. Therefore, to investigate the function of <i>QPRT</i> in Arabidopsis, we generated transgenic plants with decreased <i>QPRT</i> using the RNA interference approach. While interference of <i>QPRT</i> gene led to an impairment of NAD biosynthesis, the <i>QPRT</i> RNAi plants did not display distinguishable phenotypes under the optimal condition in comparison with wild-type plants. Intriguingly, they exhibited enhanced sensitivity to an avirulent strain of <i>Pseudomonas syringae</i> pv. <i>tomato</i> (<i>Pst-avrRpt2</i>), which was accompanied by a reduction in salicylic acid (SA) accumulation and down-regulation of pathogenesis-related genes expression as compared with the wild type. Moreover, oxidative stress marker genes including <i>GSTU24</i>, <i>OXI1</i>, <i>AOX1</i> and <i>FER1</i> were markedly repressed in the <i>QPRT</i> RNAi plants. Taken together, these data emphasized the importance of QPRT in NAD biosynthesis and immunity defense, suggesting that decreased antibacterial immunity through the alteration of NAD status could be attributed to SA- and reactive oxygen species-dependent pathways.