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Innate immune modulatory effects of elderberry polysaccharides in murine macrophage cell line RAW 264.7 (647.40)
Author(s) -
Lu ChiHua,
Lei Wei,
Fritsche Kevin
Publication year - 2014
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.28.1_supplement.647.40
Subject(s) - polysaccharide , immune system , innate immune system , tlr4 , cell culture , chemistry , ethanol precipitation , macrophage , nitric oxide , biology , microbiology and biotechnology , food science , biochemistry , immunology , in vitro , genetics , organic chemistry
Botanical‐derived polysaccharides have been suggested to modulate innate and adaptive immune responses in mammals, and elderberry consumption has also been linked to fewer sick days during cold/flu season. Therefore, we hypothesized that the immune modulatory effects of elderberry may be partially contributed by its polysaccharides. Experimental design: The polysaccharides from freeze‐dried whole elderberry (EP) were prepared by hot water and ethanol precipitation method. Intracellular reactive oxygen species (ROS), extracellular nitric oxide (NO), and gene expressions were measured from sample‐treated RAW 264.7 cells. Results: Ranging from 2 μg/mL to 30 μg/mL, EP stimulated the production of ROS/NO in a dose‐dependent manner, and the 30 μg/mL EP yielded maximum ROS/NO production as the 100 ng/mL Escherichia coli lipopolysaccharides (LPS) did. A PCR array for mouse NF‐kB pathway (PAMM‐025A, Qiagen) was used to compare the expression of 84 genes 4 hr after treatment of RAW cells with EP or LPS. Eighty of the 84 genes were found to be similarly expressed in the EP‐treated compared to LPS‐stimulated RAW cells. Conclusion: Elderberry polysaccharides stimulated immune responses in RAW 264.7 cells through NF‐kB pathway by its LPS‐like activity. Future research is undertaken to further differentiate activities of botanical polysaccharides from potential botanical endotoxins. Grant Funding Source : NIH P50AT006273