Microbial modulation of bacoside A biosynthetic pathway and systemic defense mechanism in Bacopa monnieri under Meloidogyne incognita stress.

Plant-associated beneficial microbes have been explored to fulfill the imperative function for plant health. However, their impact on the host secondary metabolite production and nematode disease management remains elusive. Our present work has shown that chitinolytic microbes viz., Chitiniphilus sp. MTN22 and Streptomyces sp. MTN14 singly as well as in combination modulated the biosynthetic pathway of bacoside A and systemic defense mechanism against Meloidogyne incognita in Bacopa monnieri. Interestingly, expression of bacoside biosynthetic pathway genes (3-Hydroxy-3-methylglutaryl coenzyme A reductase, mevalonate diphosphate decarboxylase, and squalene synthase) were upregulated in plants treated with the microbial combination in the presence as well as in absence of M. incognita stress. These microbes not only augmented bacoside A production (1.5 fold) but also strengthened host resistance via enhancement in chlorophyll a, defense enzymes and phenolic compounds like gallic acid, syringic acid, ferulic acid and cinnamic acid. Furthermore, elevated lignification and callose deposition in the microbial combination treated plants corroborate well with the above findings. Overall, the results provide novel insights into the underlying mechanisms of priming by beneficial microbes and underscore their capacity to trigger bacoside A production in B. monnieri under biotic stress.

Betulinic acid isolated from Bacopa monniera (L.) Wettst suppresses lipopolysaccharide stimulated interleukin-6 production through modulation of nuclear factor-kappaB in peripheral blood mononuclear cells.

The purpose of this study was to investigate the anti-inflammatory function and mechanism(s) of action of an active component-betulinic acid isolated from Bacopa monniera. Betulinic acid, a pentacyclic triterpenoid markedly suppressed lipopolysaccharide (LPS) induced IL-6 production in blood mononuclear cells both in vivo and in vitro. Betulinic acid also prevented LPS induced nuclear translocation of p65 NF-kappaB in hPBMCs. LPS induced nuclear translocation of NF-kappaB and IL-6 production was also abolished by p38 and ERK MAPK inhibitors PD98059 and SB203580. Addition of each of these inhibitors to cell cultures along with betulinic acid caused significant downregulation of IL-6 production and inhibition of p65 NF-kappaB nuclear translocation. The inhibitory effect of both betulinic acid and the inhibitors was higher than that of cells treated with inhibitors alone. These results suggest that betulinic acid inhibited IL-6 production by preventing p65 NF-kappaB nuclear translocation and there is a possibility that this prevention of p65 nuclear translocation may involve p38 and ERK MAPKs as cross talks occur between MAPK and NF-kappaB pathways. This study provides an insight into the probable mechanism(s) underlying the anti-inflammatory and therapeutic properties of betulinic acid.