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Project description:Rationale Microplastics are a pressing global concern and inhalation of microplastic fibers has been associated with interstitial and bronchial inflammation in flock workers. However, how microplastic fibers affect the lungs is unknown. Objectives Our aim was to assess the effects of 12x31 µm nylon 6,6 (nylon) and 15x52 µm polyethylene terephthalate (polyester) textile microplastic fibers on lung epithelial growth and differentiation. Methods We used human and murine alveolar and airway-type organoids as well as air-liquid interface cultures derived from primary lung epithelial progenitor cells and incubated these with either nylon or polyester fibers or nylon leachate. In addition, mice received one dose of nylon fibers or nylon leachate and 7 days later organoid-forming capacity of isolated epithelial cells was investigated. Results We observed that nylon microfibers, more than polyester, inhibited developing airway organoids and not established ones. This effect was mediated by components leaching from nylon. Epithelial cells isolated from mice exposed to nylon fibers or leachate, also formed fewer airway organoids, suggesting long-lasting effects of nylon components on epithelial cells. Part of these effects were recapitulated in human air-liquid interface cultures. Transcriptome analysis revealed upregulation of Hoxa5 post-exposure to nylon fibers. Inhibiting Hoxa5 protein during nylon exposure restored airway organoid formation, confirming Hoxa5's pivotal role in the effects of nylon. Conclusions These results suggest that components leaching from nylon 6,6 may especially harm developing airways and/or airways undergoing repair and we strongly encourage to characterize both hazard of and exposure to microplastic fibers in more detail.
2023-12-31 | GSE238065 | GEO
Project description:The pollution of the environment with microplastics has been recognized as an emerging threat worldwide. Due to an exponential increase in production of plastic over the last eight decades and its longevity in the environment, accumulating amounts of microplastic are polluting rivers, lakes and the ocean. Their entry pathways are diverse and still only incompletely understood. Since microplastics are usually defined smaller than 5 mm, it can be ingested by a wide range of aquatic organisms including teleost fish. There are different approaches to study the detrimental effects of pollutants on aquatic organisms. On the one hand, generic baseline parameters such as growth and mortality are regularly considered, often accompanied by established stress parameters such as cortisol, heat shock proteins or lipid oxidation. The conflicting findings to date suggest that these parameters might not be sensitive enough to indicate the physiological effects of environmentally relevant microplastic concentrations. For this reason, more sophisticated biological approaches could provide new insights into whether and how microplastics harm fish. To date, proteomic approaches have been used only sporadically when investigating the effects of microplastic exposure on aquatic organisms. So far, this approach has not been used to address potential microplastic impacts in fish. In the present study, a proteomic approach was trialed alongside established methods in an investigation of fish experiencing long-term exposure to environmentally relevant concentrations of microplastics. Two groups of rainbow trout (Oncorhynchus mykiss were exposed to microplastic concentrations and sizes currently encountered in wild fish and an increased concentration, expected to occur in the near future. These groups where compared to a control group maintained in MP free conditions. Five fish of each treatment were sampled at three time points (week 1, week 4, week 17). The experiments were performed in triplicates, resulting in 45 samples used in the proteomic analysis.
2022-08-08 | PXD033331 | Pride
Project description:Because antibiotics have been widely used to prevent severe losses due to infectious fishery diseases, the liberal application and overuse of antibiotics has led to the spread and evolution of bacterial resistance, food safety hazards, and environmental issues. The use of some antibiotics, including florfenicol and enrofloxacin, is allowed in aquaculture in China. Accordingly, to better address the concerns and questions associated with the impact of administered enrofloxacin and florfenicol to grass carp, here we investigated the immune response, bacterial diversity, and transcriptome of the intestine of C. idella treated with these oral antibiotics. The aim of this study was to provide an in-depth evaluation of the antibiotic-induced patterns and dynamics of the microbiota grass carp and the potential mechanism involved.
2022-08-08 | E-MTAB-12057 | biostudies-arrayexpress
Project description:Bactericidal antibiotics are powerful drugs because they not only inhibit essential bacterial functions, but convert them into toxic processes. Many bacteria are remarkably tolerant against antibiotics, due to inducible damage repair responses. How these responses promote whole population tolerance in important human pathogens is poorly understood. The two-component system VxrAB of the diarrheal pathogen Vibrio cholerae, a model system for tolerance against cell wall damaging (e.g., beta-lactam) antibiotics, is required for high-level beta-lactam tolerance. Here, we report the mechanism of VxrAB-mediated survival. We find that -lactam antibiotics inappropriately induce the Fur-regulated iron starvation response, causing an increase in intracellular free iron and colateral oxidative damage. VxrAB reduces antibiotic-induced toxic influx of Fe by downregulating iron importers and induces cell wall synthesis functions to counteract cell wall damage. Our results highlight the complex responses elicited by antibiotics and suggest that the ability to counteract diverse stresses promotes high-level antibiotic tolerance.
2019-07-30 | GSE135009 | GEO