Microbial growth in fresh-cut lettuce increases when wound-induced phenolic accumulation is suppressed

Abstract

Wounding lettuce (Lactuca sativa L. Longifolia) leaf mid-rib tissue initiates physiological responses that include increased synthesis and accumulation of phenolic compounds. Chlorogenic acid is the predominant wound-induced phenolic compound that accumulates in excised lettuce leaf tissue held at 10°C for 2 days. The growth of five bacterial isolates associated with lettuce decay (Erwinia carotovora, Erwinia chrisanthemi, Pseudomonas putida, Pseudomonas fluorescens, or Pseudomonas syringae) on TSA (tryptic soy agar) media was not markedly reduced by concentrations of chlorogenic acid identical to those found in wounded lettuce. Growth of E. carotovora and P. fluorescens was stimulated when prepared with TSA media containing homogenized non-wounded lettuce mid-rib tissue, while the increase was much less when the media was prepared with 5mm thick mid-rib tissue segments that were held for 2 days at 10°C after excision. Inhibiting the wound-induced increase in phenolic content with a 1-hexanol or heat-shock treatment allowed E. carotovora to grow on media prepared with excised tissue that had been held at 10°C for 2 days at significantly higher rates than on media prepared with non-treated excised tissue. Hexanol is thought to interfere with the synthesis and/or propagation of the wound signal, so delaying its application to excised mid-rib tissue reduces its effectiveness. Delaying application of the inhibitor for 4h, allowed increased accumulation of wound-induced phenolic compounds in 2 day old lettuce tissue that resulted in a concomitant reduction in the growth of E. carotovora on media prepared with this tissue. Neither the hexanol nor the heat-shock treatment themselves made the excised lettuce tissue a better substrate for microbial growth. It appears that treatments that suppress wound-induced increases in antimicrobial phenolic compounds reduce the ability of excised lettuce tissue to suppress the growth of bacteria associated with lettuce decay by limiting the production and accumulation of these antimicrobial compounds. A critical distinction is made between whether a treatment renders the tissue more susceptible to microbial growth, or whether a treatment prevents the wound-induced increase in disease resistance that limits microbial growth. If all treatments that reduce tissue browning by interfering with the wound-induced accumulation of phenolic compounds also inadvertently make the tissue more susceptible to microbial growth, then research should be directed to prevent the production of brown pigments from the wound-induced accumulated phenolic compounds, rather than devising treatments that reduce their accumulation.