Subscribe to RSS
The Majority of in vitro Macrophage Activation Exhibited by Extracts of some Immune Enhancing Botanicals is Due to Bacterial Lipoproteins and Lipopolysaccharide
We have identified potent monocyte/macrophage activating bacterial lipoproteins within commonly used immune enhancing botanicals such as Echinacea, American ginseng and alfalfa sprouts. The active lipoproteins were of the murein type and of bacterial origin since the modified amino acid 2,3 dihydroxypropyl cysteine was detected using RP-HPLC. These bacterial lipoproteins in addition to lipopolysaccharide were substantially more potent than other bacterially derived components when tested in commonly used in vitro monocyte/macrophage activation systems. In experiments using RAW 264.7 and mouse peritoneal macrophages the majority (85–98%) of the activity within extracts from eight immune enhancing botanicals was eradicated by treatment with agents (lipoprotein lipase and polymyxin B) that target these two bacterial components. Alfalfa sprouts exhibited the highest activity of those botanicals tested but the appearance of this activity during the germination of surface sterilized seeds was abolished by the presence of antibiotics. These studies indicate that the majority of the in vitro macrophage activating properties in extracts from these botanicals is due to the presence of lipoproteins and lipopolysaccharides derived from bacteria and that bacterial endophytes may be a significant source of these components. Studies using both mice and normal human volunteers suggest that these bacterial components contribute to the immune enhancing properties of orally consumed botanicals and botanical extracts. A pilot clinical trial showed that oral consumption of an extract rich in bacterial lipoproteins for one week significantly (p =.002) enhanced Natural Killer cell activity by an average of 40%. Acknowledgements: This research was partially funded by grants from the National Institutes of Health RO1 AT002360 (NCAAM) to DSP and by the USDA, Agricultural Research Service Specific Cooperative Agreement No. 58–6408–7-012.