The dysbiosis of gut microbiota is closely related to the occurrence and development of inflammatory bowel disease (IBD). The manipulation of intestinal flora through prebiotics or probiotics is expected to induce and maintain the remission of IBD symptoms. 6-week-old C57BL/J mice were daily gavaged with fructooligosaccharides (FOS) or the synbiotic two weeks before the administration of dextran sulfate sodium (DSS). The supplementation of FOS or synbiotic could significantly ameliorate the body weight loss and colon histological damage in DSS-induced acute colitis mice. The altered composition of gut microbiota in acute colitis mice was reversed by FOS or Synbiotic supplementation, with a characteristic of decreased abundance of Mucispirillum. Both FOS and synbiotic mitigated DSS-induced loss of mucus protein (MUC2) and epithelium tight junction proteins (ZO-1, Occluding, Claudin1) in colon mucosa. The expression of pro-inflammatory cytokines (IL-6 and TNF-α) was decreased by FOS or synbiotic treatment, while the expression of Tbx21 and IL-10 was increased. The results suggested that the modulation of gut microbiota by FOS or synbiotic supplementation could decrease the inflammation potential of colonized commensals, which prevented the impairment of the intestinal barrier and induced a regulation of immune response in DSS-induced acute colitis mice.

Periostin (POSTN) is a multifunctional extracellular component that regulates cell-matrix interactions and cell-cell crosstalk. POSTN deletion significantly decreases leukemia burden in mice; however, the underlying mechanisms by which POSTN promotes B cell acute lymphoblastic leukemia (B-ALL) progression remain largely unknown. Here, we demonstrate that bone marrow (BM)-derived mesenchymal stromal cells (BM-MSCs) express higher levels of POSTN when co-cultured with B-ALL cells in vitro and in vivo. POSTN deficiency in BM-MSCs significantly decreases CCL2 expression in co-cultured B-ALL cells in vitro and in vivo. Moreover, POSTN treatment increases expression of CCL2 in B-ALL cells by activating the integrin-ILK-NF-κB pathway. Conversely, CCL2 treatment upregulates expression of POSTN in BM-MSCs via STAT3 activation. Furthermore, there is a positive correlation between POSTN expression and CCL2 level in the BM of mice and patients with B-ALL. These findings suggest that B-ALL cell-derived CCL2 contributes to the increased leukemia burden promoted by BM-MSC-derived POSTN.

Bacterial infection, especially multidrug-resistant bacteria-induced infection, threatens human health seriously, which has posed great challenges for clinical therapy. The overuse of conventional antibiotics has given rise to bacterial resistance that severely restricts the clinical treatment options of conventional antibiotics. The development of highly effective antibacterial materials and therapeutic strategies to inhibit the multidrug-resistant bacteria-induced infections is of great urgency. Although silver nanoparticles (AgNPs) have exhibited certain effectiveness in killing multidrug-resistant bacteria, their antibacterial efficacy and biosafety are still unsatisfactory. In this work, we prepared graphene quantum dots (GQDs) by a green synthesis method with the natural polymer starch as a precursor for uniformly decorating AgNPs to form GQDs coated AgNPs (GQDs@Ag). The nanocomplex was comprehensively characterized, and its antibacterial activity and biosafety were systematically investigated. The characterization results revealed that the successfully constructed GQDs@Ag hybrids with improved dispersion and stability are composed of AgNPs closely and uniformly surrounded by the GQDs. Furthermore, in vitro and in vivo results demonstrated that GQDs@Ag hybrids with superior biosafety showed a markedly enhanced effect in killing MRSA and accelerating MRSA-infected wound healing as compared to AgNPs alone. Collectively, these results suggest that the biocompatible nanosystem of GQDs@Ag exhibits great potential in clinical application for MRSA infection.

Living Phanerochaete chrysosporium mycelia were used to remove heavy metals of Cd(II), Cu(II) and Zn(II) in auqeous solution. The uptake of heavy metal by the mycelia was dependent on the environmental conditions. The optimum biosorption conditions of Cd(II), Cu(II), and Zn(II) were pH 5.5–6.5 at 37°C, and 6 h. Under these conditions, the fungal biosorbent removed Cd(II), Cu(II), and Zn(II) rapidly and efficiently with maximum metal removal capacities of 59.77 mg/g, 74.78 mg/g, and 54.12 mg/g, respectively. The pseudo second-order kinetic model was superior to the pseudo first-order kinetic model, which indicated that the change of the surface sorption sites number was proportional to the square of the remaining unoccupied surface sites number. Fourier transform infrared (FT-IR) spectra indicated that hydroxyl and carboxyl groups were relevant to biosorption. Some crystal particles were found on the surface of the P. chrysosporium under scanning electron microscopy. Energy dispersive X-ray analysis and FT-IR revealed that amino acids and proteins were involved in binding metal ions. The results demonstrated that P. chrysosporium was a good potential biosorbent for adsorbing heavy metals.

Background: Activator protein 2 gamma (AP-2γ) is a member of the transcription factor activator protein-2 (AP-2) family, which is developmentally regulated and plays a role in human neoplasia. AP-2γ has been found to be overexpressed in most breast cancers, and have a dual role to inhibit tumor initiation and promote tumor progression afterwards during mammary tumorigensis. Methods: To identify the gene targets that mediate its effects, we performed chromatin immunoprecipitation (ChIP) to isolate AP-2γ binding sites on genomic DNA from human breast cancer cell line MDA-MB-453. Results: 20 novel DNA fragments proximal to potential AP-2γ targets were obtained. They are categorized into functional groups of carcinogenesis, metabolism and others. A combination of sequence analysis, reporter gene assays, quantitative real-time PCR, electrophoretic gel mobility shift assays and immunoblot analysis further confirmed the four AP-2γ target genes in carcinogenesis group: ErbB2, CDH2, HPSE and IGSF11. Our results were consistent with the previous reports that ErbB2 was the target gene of AP-2γ. Decreased expression and overexpression of AP-2γ in human breast cancer cells significantly altered the expression of these four genes, indicating that AP-2γ directly regulates them. Conclusion: This suggested that AP-2γ can coordinate the expression of a network of genes, involving in carcinogenesis, especially in breast cancer. They could serve as therapeutic targets against breast cancers in the future.