Investigations were conducted to determine the role of salicylic acid (SA) in induced systemic (ISR) resistance against blue mold disease of tobacco elicited by plant growth-promoting rhizobacteria (PGPR). SA did not inhibit germination of sporangia or development of germ tubes of Peronospora tabacina, the blue mold pathogen, in vitro. Of three PGPRstrains tested, none produced detectable levels of SA in aqueous Murashige and Skoog (MS) medium, and only Serratia marcescens strain 90-166 produced SA in tryptic soy broth (TSB). In a microtiter plate system, levels of endogenous free SA in tobacco (Nicotiana tabacum) seedlings treated with three PGPRstrains significantly increased during the first week after PGPRtreatment. In the second week, however, levels of SA were significantly lower than those in nontreated tobacco seedlings. When plants treated with Bacillus pumilus strain SE34 were challenged with P. tabacina, levels of SA increased markedly 1 day after challenge, compared to the nonbacterized and challenged control. However, a similar increase in SA 1 day after pathogen challenge did not occur in plants treated with PGPRstrains 90-166 or Pseudomonas fluorescens strain 89B-61. These observations indicate that SA accumulation in tobacco plants may play a role in ISRagainst tobacco blue mold by PGPR . Disease assays conducted in the microtiter plates showed that the tested PGPRstrains significantly reduced disease severity of blue mold in both Xanthi-nc and transgenic NahG tobacco, indicating that systemically induced resistance in tobacco to blue mold by PGPRmay be SA-independent. 2002 Elsevier Science (USA). All rights reserved.