Anti-inflammatory protein TSG-6 secreted by BMSCs attenuates silica-induced acute pulmonary inflammation by inhibiting NLRP3 inflammasome signaling in macrophages.

Silicosis is a severe occupational lung disease caused by inhalation of silica particles. Unfortunately, there are currently limited treatment options available for silicosis. Recent advances have indicated that bone marrow mesenchymal stem cells (BMSCs) have a therapeutic effect on silicosis, but their efficacy and underlying mechanisms remain largely unknown. In this study, we focused on the early phase of silica-induced lung injury to investigate the therapeutic effect of BMSCs. Our findings demonstrated that BMSCs attenuated silica-induced acute pulmonary inflammation by inhibiting NLRP3 inflammasome pathways in lung macrophages. To further understand the mechanisms involved, we utilized RNA sequencing to analyze the transcriptomes of BMSCs co-cultured with silica-stimulated bone marrow-derived macrophages (BMDMs). The results clued tumor necrosis factor-stimulated gene 6 (TSG-6) might be a potentially key paracrine secretion factor released from BMSCs, which exerts a protective effect. Furthermore, the anti-inflammatory and inflammasome pathway inhibition effects of BMSCs were attenuated when TSG-6 expression was silenced, both in vivo and in vitro. Additionally, treatment with exogenous recombinant mouse TSG-6 (rmTSG-6) demonstrated similar effects to BMSCs in attenuating silica-induced inflammation. Overall, our findings suggested that BMSCs can regulate the activation of inflammasome in macrophages by secreting TSG-6, thereby protecting against silica-induced acute pulmonary inflammation both in vivo and in vitro.

Study of thermoluminescence, photoluminescence and dosimetry for the YAGG:Ce (Y2.96Al3.4Ga1.6O12:0.04Ce) phosphor.

The comprehensive effect of ionizing radiation should be considered in the use and or analysis of certain electronic equipment. Fluorescent powders are widely used in electronic equipment, so they are attempted to be used as thermoluminescence (TL) dosimeter directly. Green YAGG:Ce phosphors were prepared by a high-temperature solid-state reaction method. The TL glow curves, TL dose response, TL three-dimensional (3D) spectra (80 K-800 K) and photoluminescence spectra for the phosphors were measured. The measurement results show that the luminescence peak temperature for the sample occurs at approximately 458 K and the luminescence peak temperatures in the TL 3D spectra are located at 130 K, 240 K and 458 K; there are four kinds of activation energies of traps in the material; the TL response of each component for the YAGG:Ce phosphor shows good linearity and the detection sensitivity of the phosphor is estimated to be less than 2 mGy. TL 3D spectra and PL spectra show that the luminescence from the phosphors arises from the 2D3/2 â†’ 2F5/2,7/2 transition of Ce ions, and the TL 3D spectra at 130 K, 240 K and 458 K are almost the same, which proves that the temperature can hardly change the relative probability of the 2D3/2 â†’ 2F5/2,7/2 transitions. The results show that YAGG:Ce could be used as dosimeter material.

Phloretin attenuates LPS-induced acute lung injury in mice via modulation of the NF-κB and MAPK pathways.

Phloretin, which can be isolated from apple trees, has demonstrable anti-inflammatory and anti-oxidant effects in macrophages. We previously reported that phloretin could inhibit the inflammatory response and reduce intercellular adhesion molecule 1 (ICAM-1) expression in interleukin (IL)-1ß-activated human lung epithelial cells. In the present study we now evaluate whether phloretin exposure could ameliorate lipopolysaccharide (LPS)-induced acute lung injury in mice. Intra-peritoneal injections of phloretin were administered to mice for 7 consecutive days, prior to the induction of lung injury by intra-tracheal administration of LPS. Our subsequent analyses demonstrated that phloretin could significantly suppress LPS-induced neutrophil infiltration of lung tissue, and reduce the levels of IL-6 and tumor necrosis factor (TNF)-α in serum and bronchoalveolar lavage fluid. We also found that phloretin modulated myeloperoxidase activity and superoxide dismutase activity, with decreased gene expression levels for chemokines, proinflammatory cytokines, and ICAM-1 in inflamed lung tissue. Phloretin also significantly reduced the phosphorylation of nuclear factor kappa B (NF-κB) and mitogen-activated protein kinase (MAPK), thus limiting the inflammatory response, while promoting expression of heme oxygenase (HO)-1 and nuclear factor erythroid 2-related factor 2, both of which are cytoprotective. Our findings suggest that, mechanistically, phloretin attenuates the inflammatory and oxidative stress pathways that accompany lung injury in mice via blockade of the NF-κB and MAPK pathways.