Oral treatment with enrofloxacin creates anti-inflammatory environment that supports induction of tolerogenic dendritic cells. 
Oral enrofloxacin treatment altered the gut microbiome promoting anti-inflammatory bacteria.  The dysbiosis promotes regulatory cell induction in the intestines and in the periphery, which suppresses contact sensitivity.  Bacterial-derived signals promote regulatory cell induction both directly and indirectly by influencing the phenotype of dendritic cells (DC).  Oral treatment with broad-spectrum antibiotic enrofloxacin was used to evaluate how gut flora perturbation shapes the immune response in the gut and the periphery.  Enrofloxacin-induced dysbiosis creates an anti-inflammatory environment characterized by increased IL-10 concentration in the gut lumen and tissues.  The production of IFN-γ and IL-17A did not change.  Oral enrofloxacin treatment skewed the profile of the immune response towards an anti-inflammatory phenotype locally in small intestinal Peyer's Patches (PP) and systematically in the spleen (SPL).  Enrofloxacin administration changed immune response in PP by increasing TGF-β secretion from an increased percentage of TGF-β-producing.  In the SPL, enrofloxacin treatment increased the secretion of TGF-β and IL-10 and decreased the secretion of IL-17A and IFN-γ.  The shift in cytokine profile correlated with a higher percentage of latency-associated peptide and IL-10-producing cells and a decreased percentage of IFN-γ-producing T cells.  This anti-inflammatory immune response in the PP and SPL promoted a higher frequency of tolerogenic DC.  Our data indicate that two-week enrofloxacin treatment induces dysbiosis, skews immune response towards an anti-inflammatory phenotype, and elevates secretion of TGF-β and IL-10 in the intestines and periphery.  Additionally, we observed higher frequencies of tolerogenic DC, characterized by CD11b and IL-10 expression, which are known inducers of Treg cells.