Sulfide induces physical damages and chemical transformation of microplastics via radical oxidation and sulfide addition.

Transformation of microplastics in aquatic environments and engineered systems (e.g., wastewater treatment plants) significantly affects their transport, fate and effects. Here, we present the counterintuitive finding that sulfide, a prevalent nucleophile and reductant, can result in oxidation of microplastics, in addition to sulfide addition. Treating four model microplastics (thermoplastic polyurethane, polystyrene, polyethylene terephthalate and polyethylene) with 0.1 mM sulfide in a Tris-buffer solution (pH 7.2, 25 °C) resulted in physical damages (embrittlement and cracking) and chemical transformation (increased O/C ratio and formation of C-S bonds) of the materials. Pre-aging of the microplastics with O3 or UV treatment had varied effects on their reactivities toward sulfide, depending on the specific structural and surface chemistry properties of the polymers. Electron paramagnetic resonance and radical trapping/quenching experiments showed that sulfide underwent spontaneous oxidation to form •OH radicals, which acted as the primary oxidant to attack the carbon atoms in the polymer chains, leading to surface oxidation and chain scission. Notably, sulfide addition, verified with X-ray photoelectron spectroscopy and 13C-nuclear magnetic resonance spectroscopy analyses, likely contributed to the physicochemical transformation of microplastics together with radical oxidation in a synergistic manner. The findings unravel an important transformation route (and a potential source) of microplastics in the environment.

Lenalidomide regulates CNS autoimmunity by promoting M2 macrophages polarization.

Multiple sclerosis (MS) is a chronic and debilitating neurological disorder of the central nervous system (CNS), characterized by infiltration of leukocytes into CNS and subsequent demyelination. Emerging evidences have revealed the beneficial roles of M2 macrophages in ameliorating experimental autoimmune encephalomyelitis (EAE), a model for MS. Here, we identify that lenalidomide alone could promote macrophages M2 polarization to prevent the progression of EAE, which is associated with subsequent inhibition of proinflammatory Th1 and Th17 cells both in peripheral lymph system and CNS. Depletion of macrophages by pharmacology treatment of clodronate liposomes or transferring lenalidomide-induced BMDMs in EAE mice completely abolished the therapeutic effect of lenalidomide or prevented EAE development, respectively. The macrophages-derived IL10 was upregulated both in vivo and in vitro after lenalidomide treatment. Moreover, lenalidomide-treated IL10-dificient EAE mice had higher clinical scores and more severe CNS damage, and intravenous injection of lenalidomide-treated IL10-/- BMDMs into mice with EAE at disease onset did not reverse disease severity, implying IL10 may be essential in lenalidomide-ameliorated EAE. Mechanistically, lenalidomide significantly increased expression and autocrine secretion of IL10, subsequently activated STAT3-mediated expression of Ym1. These studies facilitate the development of potential novel therapeutic application of lenalidomide for the treatment of MS.