Fermented botanical fertilizer controls bacterial wilt of tomatoes caused by Ralstonia pseudosolanacearum.

This study demonstrates the effect of fermented botanical product (FBP) on Ralstonia pseudosolanacearum-induced bacterial wilt disease and unravels its action mechanism. Soaking with diluted FBP solutions (0.1%-0.5%) significantly suppressed bacterial wilt in tomato plants, and FBP-treated tomato plants grew well against R. pseudosolanacearum infection. Growth assays showed that FBP had no antibacterial effect but promoted R. pseudosolanacearum growth. In contrast, few or no R. pseudosolanacearum cells were detected in aerial parts of tomato plants grown in FBP-soaked soil. Subsequent infection assays using the chemotaxis-deficient mutant (ΔcheA) or the root-dip inoculation method revealed that FBP does not affect pathogen migration to plant roots during infection. Moreover, FBP-pretreated tomato plants exhibited reduced bacterial wilt in the absence of FBP. These findings suggest that the plant, but not the pathogen, could be affected by FBP, resulting in an induced resistance against R. pseudosolanacearum, leading to a suppressive effect on bacterial wilt.

Intake of a fermented plant product attenuates allergic symptoms without changing systemic immune responses in a mouse model of Japanese cedar pollinosis.

BACKGROUND: Japanese cedar pollinosis (JCP) is one of the most prevalent allergies in Japan. Within the past few decades, many food factors have been demonstrated to suppress symptoms of pollinosis and mast cell degranulation directly or indirectly. Herein, we conducted a study to clarify the anti-allergic potency of a fermented plant product (FPP) in JCP model mice. METHODS: Mice were administered FPP, 10-fold-diluted FPP, or saline every day for 40 days by oral gavage and sensitized with major Japanese cedar pollen allergens (SBP). The numbers of sneezes were counted for 5 minutes after SBP nasal challenge. We analyzed the SBP-specific immunoglobulin titers, serum concentration of mast cell protease 1, and cytokine production from splenocytes stimulated with SBP. RESULTS: The numbers of sneezes by the mice administered FPP were significantly suppressed compared to those administered saline. The 10-fold-diluted FPP also suppressed the number of sneezes compared to saline, although not significantly. Serum level of mast cell protease 1 tended to be suppressed in FPP-consumed mice compared to those in saline-treated mice. The SBP-specific immunoglobulin titers and cytokine production were comparable among the groups. CONCLUSIONS: Our results suggest that FPP intake could attenuate JCP symptoms without change of systemic immune responses.

The regulatory mechanism of 2,4,6-trichlorophenol catabolic operon expression by HadR in Ralstonia pickettii DTP0602.

Ralstonia pickettii DTP0602 utilizes 2,4,6-trichlorophenol (2,4,6-TCP) as its sole source of carbon. The expression of catabolic pathway genes (hadA, hadB and hadC) for 2,4,6-TCP has been reported to be regulated by the LysR-type transcriptional regulator (LTTR) HadR. Generally, coinducers are recognized as being important for the function of LTTRs, and alteration of the LTTR-protection sequence and the degree of DNA bending are characteristic of LTTRs with or without a recognized coinducer. In this study, we describe the mechanism by which HadR regulates the expression of 2,4,6-TCP catabolic genes. The 2,4,6-TCP catabolic pathway genes in DTP0602 consist of two transcriptional units: hadX-hadA-hadB-hadC and monocistronic hadR. Purified HadR binds to the hadX promoter and HadR-DNA complex formation was induced in the presence of 16 types of substituted phenols, including chloro- and nitro-phenols and tribromo-phenol. In contrast with observations of other well-characterized LTTRs, the tested phenols showed no diversity of the bending angle of the HadR binding fragment. The expression of 2,4,6-TCP catabolic pathway genes, which are regulated by HadR, was not influenced by the DNA bending angle of HadR. Moreover, the transcription of hadX, hadA and hadB was induced in the presence of seven types of substituted phenols, whereas the other substituted phenols, which induced formation of the HadR-DNA complex, did not induce the transcription of hadX, hadA or hadB in vivo.