The formation of extracellular traps (ETs) has recently been recognized as a novel defense mechanism in several types of innate immune cells. It has been suggested that these structures are toxic to microbes and contribute significantly to killing several pathogens. However, the role of ETs formed by macrophages (METs) in defense against microbes remains little known. In this study, we demonstrated that a subset of murine J774A.1 macrophage cell line (8% to 17%) and peritoneal macrophages (8.5% to 15%) form METs-like structures (METs-LS) in response to Escherichia coli and Candida albicans challenge. We found only a portion of murine METs-LS, which are released by dying macrophages, showed detectable killing effects on trapped E. coli but not C. albicans. Fluorescence and scanning electron microscopy analyses revealed that, in vitro, both microorganisms were entrapped in J774A.1 METs-LS composed of DNA and microbicidal proteins such as histone, myeloperoxidase and lysozyme. DNA components of both nucleus and mitochondrion origins were detectable in these structures. Additionally, METs-LS formation occurred independently of ROS produced by NADPH oxidase, and this process did not result in cell lysis. In summary, our results emphasized that microbes induced METs-LS in murine macrophage cells and that the microbicidal activity of these METs-LS differs greatly. We propose the function of METs-LS is to contain invading microbes at the infection site, thereby preventing the systemic diffusion of them, rather than significantly killing them.

There exist complex interactions between coal and CO 2 during the process of CO 2 sequestration in coal seams with enhanced coalbed methane recovery (CO 2 -ECBM). This work concentrated on the influence of CO 2 exposure on highpressure methane and CO 2 (up to 10 MPa) adsorption behavior of three types of bituminous coal and one type of anthracite. The possible mechanism of the dependence of CO 2 exposure on adsorption performance of coal was also provided. The results indicate that the maximum methane adsorption capacities of various rank coals after CO 2 exposure increase by 3.45%−10.37%. However, the maximum CO 2 adsorption capacities of various rank coals decrease by 9.99%−23.93%. TG and pore structure analyses do not observe the obvious changes on the inorganic component and pore morphology of the coals after CO 2 exposure. In contrast, CO 2 exposure makes changes in surface chemistry of the coals, according to the results from FTIR analysis, which is the main reason for increases in the maximum adsorption capacity of methane and decreases in the maximum adsorption capacity of CO 2 for the coals after CO 2 exposure. The different role of CO 2 exposure on methane and CO 2 adsorption is detrimental to CO 2 -ECBM. Thus, the implementation of CO 2 -ECBM must take into account the influence of CO 2 exposure on the adsorption performance of the target coal seams.

BackgroundDNA methylation plays an essential role in regulating gene expression under a variety of conditions and it has therefore been hypothesized to underlie the transitions between life cycle stages in parasitic nematodes. So far, however, 5'-cytosine methylation has not been detected during any developmental stage of the nematode Caenorhabditis elegans. Given the new availability of high-resolution methylation detection methods, an investigation of life cycle methylation in a parasitic nematode can now be carried out.ResultsHere, using MethylC-seq, we present the first study to confirm the existence of DNA methylation in the parasitic nematode Trichinella spiralis, and we characterize the methylomes of the three life-cycle stages of this food-borne infectious human pathogen. We observe a drastic increase in DNA methylation during the transition from the new born to mature stage, and we further identify parasitism-related genes that show changes in DNA methylation status between life cycle stages.ConclusionsOur data contribute to the understanding of the developmental changes that occur in an important human parasite, and raises the possibility that targeting DNA methylation processes may be a useful strategy in developing therapeutics to impede infection. In addition, our conclusion that DNA methylation is a mechanism for life cycle transition in T. spiralis prompts the question of whether this may also be the case in any other metazoans. Finally, our work constitutes the first report, to our knowledge, of DNA methylation in a nematode, prompting a re-evaluation of phyla in which this epigenetic mark was thought to be absent.

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