Fe/S Redox-Coupled Mercury Transformation Mediated by Acidithiobacillus ferrooxidans ATCC 23270 under Aerobic and/or Anaerobic Conditions.

Bioleaching processes or microbially mediated iron/sulfur redox processes in acid mine drainage (AMD) result in mineral dissolution and transformation, the release of mercury and other heavy metal ions, and changes in the occurrence forms and concentration of mercury. However, pertinent studies on these processes are scarce. Therefore, in this work, the Fe/S redox-coupled mercury transformation mediated by Acidithiobacillus ferrooxidans ATCC 23270 under aerobic and/or anaerobic conditions was studied by combining analyses of solution behavior (pH, redox potential, and Fe/S/Hg ion concentrations), the surface morphology and elemental composition of the solid substrate residue, the Fe/S/Hg speciation transformation, and bacterial transcriptomics. It was found that: (1) the presence of Hg2+ significantly inhibited the apparent iron/sulfur redox process; (2) the addition of Hg2+ caused a significant change in the composition of bacterial surface compounds and elements such as C, N, S, and Fe; (3) Hg mainly occurred in the form of Hg0, HgS, and HgSO4 in the solid substrate residues; and (4) the expression of mercury-resistant genes was higher in earlier stages of growth than in the later stages of growth. The results indicate that the addition of Hg2+ significantly affected the iron/sulfur redox process mediated by A. ferrooxidans ATCC 23270 under aerobic, anaerobic, and coupled aerobic-anaerobic conditions, which further promoted Hg transformation. This work is of great significance for the treatment and remediation of mercury pollution in heavy metal-polluted areas.

Complement protein C5a enhances the ß-amyloid-induced neuro-inflammatory response in microglia in Alzheimer's disease.

OBJECTIVE: The dysregulation of neuro-inflammation is one of the attributes of the pathogenesis of Alzheimer's disease (AD). Over-expression of complement proteins co-localizes with neurofibrillary tangles, thereby indicating that a complement system may be involved in neuro-inflammation. Here, we report the influence of complement activation on the neuro-inflammation using a microglial cell line. METHODS: first, we performed a cytotoxic assay using the microglial cells BV-2. Second, after treatment of BV-2 cells with Aß42 and/ or C5a, the anaphylatoxin derived from C5, we determined the expression levels of the pro-inflammatory factors TNF-α, IL-1ß, and IL-6. Finally, we explored whether this neuroinflammatory response was mediated by JAK/ STAT3 signaling. RESULTS: C5a had an enhanced effect on the neural cell viability of BV-2 cells treated with Aß42. In addition, C5a also increased the Aß-induced neuro-inflammatory response, and these effects were blocked by the C5aR antagonist, PMX205. Finally, we demonstrated that the neuro-inflammatory responses induced by Aß and C5a were mediated through JAK/STAT3 signaling. By blocking this pathway with an antagonist, AG490, the expression of TNF-α, IL-1ß, and IL-6 was alleviated. CONCLUSION: The complement protein C5a could exaggerate the Aß-induced neuroinflammatory response in microglia, and C5aR may be a potential therapeutic tool for AD treatment.