Enhanced degradation of polyethylene terephthalate plastics by CdS/CeO2 heterojunction photocatalyst activated peroxymonosulfate.

Waste plastics have posed enormous to the environment, but their recycling, especially polyethylene terephthalate plastics, was still a huge challenge. Here, CdS/CeO2 was used as the photocatalyst to promote the degradation of PET-12 plastics by activating peroxymonosulfate (PMS) synergistic photocatalytic system. The results showed that 10 % CdS/CeO2 had the best performance under the illumination condition, and the weight loss rate of PET-12 could reach 93.92 % after adding 3 mM PMS. The effects of important parameters (PMS dose and co-existing anions) on PET-12 degradation were systematically studied, and the excellent performance of the photocatalytic-activated PMS system was verified by comparison experiments. SO4•- contributed the most to the degradation performance of PET-12 plastics, which was demonstrated by electron paramagnetic resonance (EPR) and free radical quenching experiments. Furthermore, the results of GC showed that the gas products including CO, and CH4. This indicated that the mineralized products could be further reduced to hydrocarbon fuel under the action of the photocatalyst. This job supplied a new idea for the photocatalytic treatment of waste microplastics in the water, which will help recycle waste plastics and recycle carbon resources.

Responses of CD27+ CD38+ plasmablasts, and CD24hi CD27hi and CD24hi CD38hi regulatory B cells during primary dengue virus 2 infection.

BACKGROUND: Humoral immunity is thought to play a central role in mediating the immunopathogenesis of dengue virus (DENV) infection; however, the B-cell responses elicited by primary DENV2 infection are incompletely understood. Follicular helper T cells (Tfh) are important to promote B-cell activation and differentiation. METHODS: The present study analyzed the detailed dynamic changes of circulating B-cell subsets and Tfh (cTfh) using flow cytometry to explore their responses to DENV2 infection. RESULTS: Thirty-six patients with DENV2 and 21 healthy individuals were included. The results showed that CD27+ CD38+ plasmablasts emerged after DENV2 infection, and correlated with CXCR5+ PD-1+ or CXCR5+ ICOS+ PD-1+ cTfh, which increased after DENV2 infection, and correlated with DENV2 RNA viral loads. Significantly low levels of CD27- naïve B cells, and CD24hi CD27hi and CD24hi CD38hi regulatory B cells (Breg) were observed after DENV2 infection, which correlated negatively with CXCR5+ PD-1+ or CXCR5+ ICOS+ PD-1+ cTfh cells. CONCLUSION: Overall, these results provide insights into the DENV2-elicited B-cell response and revealed previously unidentified CD24hi CD27hi and CD24hi CD38hi Breg responses to DENV2 infection.

IP3R and RyR channels are involved in traffic-related PM2.5-induced disorders of calcium homeostasis.

Traffic-related PM2.5 can result in immune system damage and diseases; however, the possible mechanism of its effect remains unclear. Calcium (Ca2+) is a critical signaling molecule in a variety of cells. Indeed, Ca2+ is involved in numerous basic functions, including cell growth and death. In this study, Jurkat T cells were used to explore the possible mechanisms of PM2.5-elicited intracellular Ca2+signal responses. The results indicate that PM2.5 could raise the level of intracellular Ca2+ concentration ([Ca2+]i). The [Ca2+]i in Jurkat T cells significantly decreased after treatment with heparin as an inhibitor of inositol trisphosphate receptors (IP3 R), or procaine as an inhibitor of ryanodine receptors (RyR). The expression of calmodulin (CAM) protein decreased in a time-dependent manner after exposure to PM2.5, whereas the activity of Ca2+-Mg2+-ATPase seemed to show a slight drop trend after exposure to PM2.5. Our findings demonstrate that PM2.5 stimulation to Jurkat T cells would result in an increase in [Ca2+]i, which is modulated by IP3 R and RyR, as well as CAM.

Protective role of follicular CXCR5+CD8+ T cells against dengue virus 2 infection.

Follicular CXCR5+CD8+ T cells have antiviral effects in chronic virus infection, but the roles of these cells during dengue virus 2 (DENV2) infection remain poorly understood. OBJECTIVE: This study was conducted to analyzed in detail the dynamic changes and functional properties of circulating follicular CXCR5+CD8+ T cells to explore their effects on DENV2 infection. METHODS: Circulating follicular CXCR5+CD8+ T cells and cytokines were analyzed by flow cytometry in DENV2 patients at difference days after DENV2 infection. CD8+ T cells were isolated and purified from DENV2 patients, then were stimulated with NS1 peptides and TCR stimulant. After cultivation, multiple parameters were tested. RESULTS: (1) CXCR5+CD8+ T cells emerged after DENV2 infection, with high PD-1 expression, and were correlated with the reduction in DENV2 RNA viral loads. (2) PD-1+CXCR5+CD8+ T cells were negatively associated with disease progression. (3) Serum IFN-γ, IL-6 and IL-10 levels were increased late in the course of DENV2 infection. (4) CXCR5+CD8+ T cells from DENV2 patients exhibited increased cytotoxicity and IFN-γ and IL-10 secretion. CONCLUSION: CXCR5+CD8+ T cells could play a protective role in dengue pathogenesis and may be a novel strategy for controlling DENV2 infection and vaccine development.

Traffic-related PM2.5 induces cytosolic [Ca²âº] increase regulated by Orai1, alters the CaN-NFAT signaling pathway, and affects IL-2 and TNF-α cytoplasmic levels in Jurkat T-cells.

The atmospheric particulate matter with a diameter less than or equal to 2.5 um (PM2.5) can result in increased immune system damage or diseases, however, the possible mechanism remains unclear. In this study, we used Jurkat T cells to determine the effects of PM2.5 on T cell-mediated adaptive immune response. Our results indicated that PM2.5 exposure increased intracellular calcium ion concentration [Ca(2+)]. In contrast, cytosolic free Ca(2+) concentration [Ca(2+)]i significantly decreased in Jurkat T cells transfected with Orai1siRNA. In addition, we detected the level of interleukin (IL)-2 and tumor-necrosis factor (TNF)-α as well as other signalling molecules, including calcineurin (CaN) and NFATc2, a gene on 20q13.2 that encodes a member of the nuclear factor of activated T cells (NFAT), in the supernatant of cells exposed to PM2.5. The expression of NFATc2 protein increased in a time-dependent manner after exposure to PM2.5, but the activity of CaN decreased. NFATc2 was not consistent with IL-2 accumulation, thus indicating the involvement of other signals in the suppression of IL-2 accumulation. Our findings demonstrate that PM2.5 exposure in immune cells results in locally increased [Ca(2+)]i generated by Orai1 and CaN-NFAT gene expression, TNF-α and IL-2 cytoplasmic concentrations may be altered.