A polystyrene (PS)-anchored Pd(II) metal complex was synthesized on cross-linked polymer by heating a mixture of chlorometylated polystyrene with phenyldithiocarbazate and carbon disulfide in the presence of potassium hydroxide (KOH) in dimethylformamide (DMF). The reaction mixture was heated at 80 °C to form the corresponding phenyldithiocarbazate-functionalized polymer. Then, it was treated with bis(benzonitrile)palladium(II) chloride. The properties of dark colored polymer, impregnated with the metal complex was then characterized by various spectroscopic technique such as Fourier Transform Infrared (FTIR), Scanning Electron Microscopy/Energy Dispersive X-ray (SEM/EDX), CHNS elemental analysis, BET surface area, X-ray Diffraction (XRD), Thermogravimetric (TGA) and Inductively Coupled Plasma-Optical Emission (ICP-OES) spectroscopy.
Synthetic glycine coated 50 nm polystyrene nanoparticles (NP) (PS50G), unlike ambient NP, do not promote pulmonary inflammation, but instead, render lungs resistant to the development of allergic airway inflammation. In this study, we show that PS50G modulate the frequency and phenotype of regulatory T cells (Treg) in the lung, specifically increasing the proportion of tumor necrosis factor 2 (TNFR2) expressing Treg. Mice pre-exposed to PS50G, which were sensitized and then challenged with an allergen a month later, preferentially expanded TNFR2+Foxp3+ Treg, which further expressed enhanced levels of latency associated peptide and cytotoxic T-lymphocyte associated molecule-4. Moreover, PS50G-induced CD103+ dendritic cell activation in the lung was associated with the proliferative expansion of TNFR2+Foxp3+ Treg. These findings provide the first evidence that engineered NP can promote the selective expansion of maximally suppressing TNFR2+Foxp3+ Treg and further suggest a novel mechanism by which NP may promote healthy lung homeostasis.