Figure 2
From: The cytosolic sensor STING is required for intestinal homeostasis and control of inflammation
Activation of STING (stimulator of interferon genes) by commensals. (a) Confocal microscopy of wild-type (WT) murine embryonic fibroblasts (MEFs) stained with anti-STING and DAPI (4,6-diamidino-2-phenylindole), unstimulated or stimulated for 4 h with STING-activating dsDNA (dsDNA90 base pairs), fecal content, or microbiota DNA purified from feces from WT mice. MEFs from STING−/− mice did not stain with anti-STING (data not shown). Arrows highlight STING punctual aggregation. (b) Quantitative reverse transcriptase–PCR (qRT–PCR) analysis of interferon (IFN)-β mRNA in the colons from WT or STING−/− mice. Data represent two independent experiments with four mice per group. (c) qRT–PCR analysis of IFN-β mRNA in the colons from WT or STING−/− mice treated with a broad spectrum of antibiotics. (d) qRT–PCR analysis of IFN-β mRNA of WT and STING−/− mice lamina propria cell culture stimulated with STING-activating dsDNA or microbiota DNA purified from feces for 16 h. (e) Distribution of operational taxonomic units in feces from WT and STING−/− mice. Assessment of structure of microbial communities by (f) weighted and (g) unweighted UniFrac principal coordinate analyses (PCoA) plots are presented for gut bacteria sequenced. Distribution of bacteria phyla in feces from (h) WT and (i) STING−/− mice evidencing main differences within each phylum. Data represent two independent experiments with three to five mice per group. Data represent the mean±s.e.m. *P<0.05; ####P<0.0001.
