The role of Fusobacterium nucleatum, often associated with intestinal diseases, in remission of dextran sulfate sodium (DSS)-induced colitis was investigated. Female mice were divided into groups DC (DSS control) and DF (DSS + F.nucleatum). F.nucleatum (1.0 × 1010 cfu/mouse/day) in PBS was orally given to DF, while DC had PBS only. All mice had DSS in drinking water. In Experiment 1, mice underwent two inflammation phases, an in-between recovery phase, and had their disease activity indices (DAI) calculated. Experiment 2 was similarly conducted, except that mice were dissected 3 days post-recovery, and had blood and colonic mucosal samples collected. In Experiment 1, DF had significantly (P < .05) higher DAI than DC, during the recovery and 2nd inflammation phases. In Experiment 2, genus Bacteroides was significantly (P < .05) higher and family Lachnospiraceae significantly lower in cecal mucosa-associated microbiota of DF than in that of DC. We concluded that F.nucleatum can impeded colitis remission.

We previously reported that the major component of Enterococcus faecalis strain EC-12 (EC-12) inducing production of Interleukin (IL)-12 in mouse/human immune cells was its own RNA. This study aimed to investigate if RNase A-treated EC-12 could also produce IL-10 and to evaluate the possible effects of IL-10 produced by RNase A-treated EC-12. Three experiments were conducted: (1) Assessment of the effect of RNase A-treated EC-12 on transcriptome profiles and biological pathways in human peripheral blood mononuclear cells; (2) Determination of cytokine concentration in its culture supernatants; and (3) Supplementation of RNase A-treated EC-12 (RN) to mice with dextran sodium sulfate-induced colitis. Treatment of EC-12 with RNase A inhibited inflammatory response including the potency to induce IL-12 production, while it did not affect IL-10 production (Experiment 1 and 2). Colitis symptoms were milder in RN than in PBS-supplemented controls (Experiment 3). RNase A-treated EC-12 likely became an anti-inflammatory agent primarily inducing IL-10 production.