RESUMEN
Antibiotics and heavy metals have caused serious contamination of the environment and even resulted in public health concerns. It has therefore become even more urgent to adopt a sustainable approach to combating these polluted environments. In this paper, we investigated the microbial community of marine sediment samples after 255 days of enrichment culture under Cu (II) and lincomycin stress and ZC255 was the most resistant strain obtained. The 16S rRNA gene sequence confirmed that it belonged to the genus Rossellomorea. Strain ZC255 was resistant to 12 kinds of antibiotics, and had a superior tolerance to Cu (II), Pb (II), Ni (II), Zn (II), Cr (III), and Cd (II). Moreover, it exhibits strong bioremoval ability of Cu and lincomycin. The removal efficiency of Cu (II) and lincomycin can achieve 651 mg/g biomass and 32.5 mg/g biomass, respectively. Strain ZC255 was a promising isolate for pollution bioremediation applications.
RESUMEN
Glucocorticoids (GC) are the most commonly prescribed medications for patients with inflammatory diseases, despite their well-known adverse metabolic effects. Previously, it was understood that the anti-inflammatory effects of the GC/GC receptor (GR) complex were mediated via transrepression, whilst the adverse metabolic effects were mediated via transactivation. It has recently become clear that this "divergent actions" paradigm of GC actions is likely insufficient. It has been reported that the GC/GR-mediated transactivation also contributes to the anti-inflammatory actions of GC, via up-regulation of key anti-inflammatory proteins. One of these is glucocorticoid-induced leucine zipper (GILZ), which inhibits inflammatory responses in a number of important immune cell lineages in vitro, as well as in animal models of inflammatory diseases in vivo. This review aims to compare the GILZ and GC effects on specific cell lineages and animal models of inflammatory diseases. The fact that the actions of GILZ permit a GILZ-based gene therapy to lack GC-like adverse effects presents the potential for development of new strategies to treat patients with inflammatory diseases.
RESUMEN
OBJECTIVE: Glucocorticoid-induced leucine zipper (GILZ) is a glucocorticoid-induced protein, the reported molecular interactions of which suggest that it functions to inhibit inflammation. However, the role of endogenous GILZ in the regulation of inflammation in vivo has not been established. This study was undertaken to examine the expression and function of GILZ in vivo in collagen-induced arthritis (CIA), a murine model of rheumatoid arthritis (RA), and in RA synoviocytes. METHODS: GILZ expression was detected in mouse and human synovium by immunohistochemistry and in cultured cells by real-time polymerase chain reaction and permeabilization flow cytometry. GILZ function was assessed in vivo by small interfering RNA (siRNA) silencing using cationic liposome-encapsulated GILZ or control nontargeting siRNA and was assessed in vitro using transient overexpression. RESULTS: GILZ was readily detectable in the synovium of mice with CIA and was up-regulated by therapeutic doses of glucocorticoids. Depleting GILZ expression in vivo increased the clinical and histologic severity of CIA and increased synovial expression of tumor necrosis factor and interleukin-1 (IL-1), without affecting the levels of circulating cytokines or anticollagen antibodies. GILZ was highly expressed in the synovium of patients with active RA and in cultured RA synovial fibroblasts, and GILZ overexpression in synovial fibroblasts inhibited IL-6 and IL-8 release. CONCLUSION: Our findings indicate that GILZ functions as an endogenous inhibitor of chronic inflammation via effects on cytokine expression and suggest that local modulation of GILZ expression could be a beneficial therapeutic strategy.
