Human monocytes downregulate innate response receptors following exposure to the microbial metabolite n-butyrate.
Felix LasitschkaThomas GieseMarco PaparellaStefan R KurzhalsGuido WabnitzKatrin JacobJudith GrasKonrad A BodeAnne-Kristin HeningerTimea SziskzaiYvonne SamstagCornelia LeszinskiBettina JocherMohammed Al-SaeediStefan C MeuerJutta Schröder-BraunsteinPublished in: Immunity, inflammation and disease (2017)
In summary, the intestinal microbiota may support symbiosis with the human host organism by n-butyrate mediated downregulation of protein and gene expression of innate response receptors as well as xCT on circulating monocytes following recruitment to the lamina propria. Downregulation of CD16 gene expression may at least partially be caused at the transcriptional level by the n-butyrate mediated decrease in expression of the transcription factor PU.1 in circulating monocytes.
Keyphrases
- gene expression
- transcription factor
- immune response
- endothelial cells
- dendritic cells
- dna methylation
- induced pluripotent stem cells
- peripheral blood
- cell proliferation
- signaling pathway
- poor prognosis
- pluripotent stem cells
- microbial community
- small molecule
- oxidative stress
- long non coding rna
- heat shock protein
- genome wide identification