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Effect of dietary abscisic acid (ABA) supplementation on spleen transcriptome in LPS-challenged mice

ABSTRACT: BACKGROUND: Dietary ABA-supplementation modulates immune and inflammatory responses in mouse models of chronic and infectious disease. However, the underlying mechanisms by which ABA elicits its immune modulatory effects are not well understood. This project used a systems approach in combination with functional and in vivo studies to investigate the target gene pathways modulated by ABA in the context of an inflammatory LPS challenge. RESULTS: Dietary ABA-supplementation regulates the expression of gene pathways associated with peroxisome proliferator-activated receptor gamma (PPAR g), cAMP signaling and lipid metabolism in PPAR g-expressing mice. However, the pattern of differentially expressed genes is significantly reduced in the spleens of tissue-specific PPAR g null mice fed ABA. These differences in gene expression coincided with enhanced PPAR g-reporter activity of macrophages treated with ABA and enhanced intracellular cAMP accumulation in ABA-treated splenocytes.

ORGANISM(S): Mus musculus

PROVIDER: GSE21013 | GEO | 2010/09/01

SECONDARY ACCESSION(S): PRJNA125755

REPOSITORIES: GEO

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Effect of dietary abscisic acid (ABA) supplementation on spleen transcriptome in LPS-challenged mice

Project description:BACKGROUND: Dietary ABA-supplementation modulates immune and inflammatory responses in mouse models of chronic and infectious disease. However, the underlying mechanisms by which ABA elicits its immune modulatory effects are not well understood. This project used a systems approach in combination with functional and in vivo studies to investigate the target gene pathways modulated by ABA in the context of an inflammatory LPS challenge. RESULTS: Dietary ABA-supplementation regulates the expression of gene pathways associated with peroxisome proliferator-activated receptor gamma (PPAR g), cAMP signaling and lipid metabolism in PPAR g-expressing mice. However, the pattern of differentially expressed genes is significantly reduced in the spleens of tissue-specific PPAR g null mice fed ABA. These differences in gene expression coincided with enhanced PPAR g-reporter activity of macrophages treated with ABA and enhanced intracellular cAMP accumulation in ABA-treated splenocytes. Splenocytes from wild-type (WT) and Null (epithelial and immune cell-specific PPARg knock-out) mice were sampled with or without ABA supplementation and with or without LPS stimulation.

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