Fig. 2: Oxicam compounds inhibit SA-dependent immunity.

a Chemical structures of salicylic acid (SA), tenoxicam (TNX), meloxicam (MLX), and piroxicam (PRX). b, c Col-0 WT plants were syringe-infiltrated with (+) or without (−) 1 × 10⁵ cfu/mL Pto suspension in the presence (+) or absence (−) of 100 µM TNX for 24 h. PR1 (b) and PDF1.2 (c) transcript levels were measured by qRT-PCR with cDNA prepared from each of the samples. The expression values of individual genes were normalized against ACT2. Data are shown as means ± SE of three independent experiments, each with three replicates. Different letters indicate significant differences (two-sided Tukey–Kramer test, p < 0.05). d Col-0 WT seedlings were treated with TNX for 1 h before treatment with 100 μM SA (+) or water (−) for 24 h. PR1 transcript levels were measured by qRT-PCR. Expression values were normalized against ACT2. Data are shown as means ± SE of three independent experiments, each with three replicates. Different letters indicate significant differences (two-sided Tukey–Kramer test, p < 0.05). e PR1p:GUS seedlings were treated with indicated concentration of oxicam derivatives (TNX, MLX, or PRX) or 0.5% DMSO control for 1 h before treatment with 100 μM SA (+) or water (−). GUS activity was measured after 24 h. Data are shown as means ± SE (n = 3 biological replicates). Asterisks indicate significant differences from 100 µM SA alone (two-sided Dunnett test, p < 0.05). f Col-0 WT, sid2-2, and npr1-1 plants were syringe-infiltrated with 1 × 10⁵ cfu/mL of Pto suspension in 10 mM MgCl₂ and 0.25% DMSO in the presence (+) or absence (−) of 100 μM TNX. Bacterial growth was determined 3 days-post-inoculation. Data are shown as means ± SE (n = 6 biological replicates). Different letters indicate significant differences (two-sided Tukey–Kramer test, p < 0.05). In e and f, experiments were repeated three times with similar results.