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Imbalance of gut microbiota homeostasis is related to the occurrence of ulcerative colitis (UC), and probiotics are thought to modulate immune microenvironment and repair barrier function. Here, in order to reveal the interaction between UC and gut microbiota, we screened a new probiotic strain by 16S rRNA sequencing from Dextran Sulfate Sodium (DSS)-induced colitis mice, and explored the mechanism and clinical relevance. Lactobacillus johnsonii (L. johnsonii), as a potential anti-inflammatory bacterium was decreased colonization in colitis mice. Gavage L. johnsonii could alleviate colitis by specifically increasing the proportion of intestinal macrophages and the secretion of Il-10 with macrophages depleted model and in Il10−/− mice. We identified this subset of immune cells activated by L. johnsonii as CD206+ macrophagesIL−10. Mechanistically, L. johnsonii supplementation enhanced the mobilization of CD206+ macrophagesIL−10 through the activation of STAT3 in vivo and in vitro. In addition, we revealed that TLR1/2 was essential for the activation of STAT3 and the recognition of L. johnsonii by macrophages. Clinically, there was positive correlation between the abundance of L. johnsonii and the expression level of MRC1, IL10 and TLR1/2 in UC tissues. L. johnsonii could activate native macrophages into CD206+ macrophages and release IL-10 through TLR1/2-STAT3 pathway to relieve experimental colitis. L. johnsonii may serve as an immunomodulator and anti-inflammatory therapeutic target for UC.

Antibiotics in ecosystems stimulate the emergence and development of antibiotic-resistant bacteria and genes, consequently posing tremendous health risks to wildlife species and humans. Laccase, a multicopper-containing oxidoreductase, is capable of nonspecifically catalyzing oxidization of multiple hazardous micropollutants, including antibiotics, with O2 as the terminal electron acceptor. Thus, laccase is recognized as a promising "green and sustainable biocatalyst" for the decontamination of antibiotics. Recently, great efforts have been made to design and exploit immobilized laccase to tackle antibiotics in the environment. In this review, the occurrence, fate, and ecological risks of antibiotics in environmental matrices are described. Moreover, the immobilized laccase-evoked removal of antibiotics, owing to immobilization technology reinforcing the stability and reusability of free laccase in bioremediation, is examined in details. In particular, advances in laccase-provoked transformation mechanisms (i.e. oxidative decomposition and radical polymerization) of antibiotics are highlighted, and a valuable guideline beneficial to large-scale practical applications is provided. Furthermore, evaluation of the intermediate products of antibiotics and their ecotoxicity in different laccase-enabled treatments is summarized. Finally, new directions for the application of laccase for effective antibiotic removal are envisaged, and several future directions to address the challenges are proposed. [ABSTRACT FROM AUTHOR]

The vibrational, mechanical, electronic, and optical properties of the ε-O8 phase in the pressure range of 11.4–70 GPa were studied by the first-principle calculation method. The phonon dispersion curves have a tiny virtual frequency at 60 GPa, which indicates that ε-O8 is dynamically unstable at 60 GPa. However, the 3-BM EOS demonstrates that the unit cell is stable up to 70 GPa. It has been shown that ε-O8 remains ductile within the whole applied pressure range. Concurrently, we calculated the variation of the band gap of ε-O8 in the pressure range of 11.4–70 GPa. The results show that the band gap of ε-O8 decreases with increasing pressure. Notably, the band gap disappears within the range of 50–60 GPa, which reveals that the metallic phase transition occurs within this pressure range. [ABSTRACT FROM AUTHOR]

Background: Severe acute pancreatitis (SAP) is a deadly inflammatory disease with complex pathogenesis and lack of effective therapeutic options. N 6 -methyladenosine (m 6 A) modification of circRNAs plays important roles in physiological and pathological processes. However, the roles of m 6 A circRNA in the pathological process of SAP remains unknown., Aim: To identify transcriptome-wide map of m 6 A circRNAs and to determine their biological significance and potential mechanisms in SAP., Methods: The SAP in C57BL/6 mice was induced using 4% sodium taurocholate salt. The transcriptome-wide map of m 6 A circRNAs was identified by m 6 A-modified RNA immunoprecipitation sequencing. The biological significance of circRNAs with differentially expressed m 6 A peaks was evaluated through gene ontology and Kyoto Encyclopedia of Genes and Genomes analysis. The underlying mechanism of m 6 A circRNAs in SAP was analyzed by constructing of m 6 A circRNA-microRNA networks. The expression of demethylases was determined by quantitative polymerase chain reaction and western blot to deduce the possible mechanism of reversible m 6 A process in SAP., Results: Fifty-seven circRNAs with differentially expressed m 6 A peaks were identified by m 6 A-modified RNA immunoprecipitation sequencing, of which 32 were upregulated and 25 downregulated. Functional analysis of these m 6 A circRNAs in SAP found some important pathways involved in the pathogenesis of SAP, such as regulation of autophagy and protein digestion. In m 6 A circRNA-miRNA networks, several important miRNAs participated in the occurrence and progression of SAP were found to bind to these m 6 A circRNAs, such as miR-24-3p, miR-26a, miR-92b, miR-216b, miR-324-5p and miR-762. Notably, the total m 6 A level of circRNAs was reduced, while the demethylase alkylation repair homolog 5 was upregulated in SAP., Conclusion: m 6 A modification of circRNAs may be involved in the pathogenesis of SAP. Our findings may provide novel insights to explore the possible pathogenetic mechanism of SAP and seek new potential therapeutic targets for SAP., Competing Interests: Conflict-of-interest statement: The authors declare that there is no conflict of interest related to this study., (©The Author(s) 2021. Published by Baishideng Publishing Group Inc. All rights reserved.)