Journal
FOOD RESEARCH INTERNATIONAL
Volume 144, Issue -, Pages -Publisher
ELSEVIER
DOI: 10.1016/j.foodres.2021.110310
Keywords
RNA-seq; Caco-2; Ganoderma atrum polysaccharides; Caco-2; DCs co-culture model
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Funding
- National Natural Science Foundation of China [81760737]
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In this study, it was found that Ganoderma atrum polysaccharide (PSG-1) indirectly affects dendritic cells' immune function in the intestinal-like Caco-2/DCs co-culture model. The interaction between Caco-2 and DCs was regulated by PSG-1 through TNF-alpha and NF-kappa B signaling pathways of Caco-2 in the model. This suggests a potential mechanism for immune modulation in the gut environment through interactions between intestinal epithelial cells and immune cells.
The previous research has indicated that Ganoderma atrum polysaccharide (PSG-1) indirectly affects the immune function of dendritic cells (DCs) in intestinal-like Caco-2/DCs co-culture model, in which NF-kappa B and MAPK pathway play an essential role. To explore the interaction of Caco-2 in the interaction between the intestinal epithelium and its internal immune cells, the intestinal-like Caco-2/DCs co-culture model was developed. All transcripts of Caco-2 treated with or without PSG-1 were globally screened by RNA-seq. The expression of 452 genes regulated by PSG-1 was statistically significant, the counts of up-regulated and down-regulated genes were 198 and 256, respectively. According to KEGG analysis, tumor necrosis factor (TNF)-alpha and NF-kappa B signaling pathways of Caco-2 were selected to elucidate the mechanism of interaction between Caco-2/DCs induced by PSG-1. After the addition of TNF-alpha inhibitor Apremilast and NF-kappa B inhibitor BAY11-70821 in Caco-2, expression of cytokines (TNF-alpha, IL-6, IL-1 beta, IL-10), chemokines (RANTES, MIP-1 alpha, MCP-1), and the key proteins of MAPK and NF-kappa B pathways of DCs were all reduced. In summary, dialogue between Caco-2 and DCs was regulated by PSG-1 through TNF-alpha and NF-kappa B signaling pathways of Caco-2 in the model.
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