Conductive magnetite nanoparticles trigger syntrophic methane production in single chamber microbial electrochemical systems.

Performance of methane-producing microbial electrochemical systems (MESs) is highly reliant on electron transfer efficiency from electrode to microorganisms and vice versa. In this study, magnetite nanoparticles were used as electron carriers to enhance extracellular electron transfer in single chamber MESs. The MES with magnetite exhibited the highest methane yield and current generation of 0.37 ±â€¯0.009 LCH4/gCOD and 9.6 mA, respectively among the tested reactors. The experimental data was observed to be highly consistent with modified Gompertz model results (R2 > 0.99), which also showed 74.2% and 22.1% enhanced methane production rate in MES with magnetite as compared to control AD and MES without magnetite, respectively. Cyclic voltammetry and electrochemical impedance spectroscopy analysis confirmed that magnetite enhanced catalytic activity of biofilm and lowered both solution and charge transfer resistance. Therefore, supplementing magnetite in MESs could be a strategy to develop an efficient syntrophic biomethanation in field scale applications.

Treg-specific IL-27Rα deletion uncovers a key role for IL-27 in Treg function to control autoimmunity.

Dysregulated Foxp3+ Treg functions result in uncontrolled immune activation and autoimmunity. Therefore, identifying cellular factors modulating Treg functions is an area of great importance. Here, using Treg-specific Il27ra-/- mice, we report that IL-27 signaling in Foxp3+ Tregs is essential for Tregs to control autoimmune inflammation in the central nervous system (CNS). Following experimental autoimmune encephalomyelitis (EAE) induction, Treg-specific Il27ra-/- mice develop more severe EAE. Consistent with the severe disease, the numbers of IFNγ- and IL-17-producing CD4 T cells infiltrating the CNS tissues are greater in these mice. Treg accumulation in the inflamed CNS tissues is not affected by the lack of IL-27 signaling in Tregs, suggesting a functional defect of Il27ra-/- Tregs. IL-10 production by conventional CD4 T cells and their CNS accumulation are rather elevated in Treg-specific Il27ra-/- mice. Analysis with Treg fate-mapping reporter mice further demonstrates that IL-27 signaling in Tregs may control stability of Foxp3 expression. Finally, systemic administration of recombinant IL-27 in Treg-specific Il27ra-/- mice fails to ameliorate the disease even in the presence of IL-27-responsive conventional CD4 T cells. These findings uncover a previously unknown role of IL-27 in regulating Treg function to control autoimmune inflammation.