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      Microplastics-perturbed gut microbiota triggered the testicular disorder in male mice: Via fecal microbiota transplantation

      , , , , ,
      Environmental Pollution
      Elsevier BV

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          Abstract

          Microplastics (MPs), an emerging environmental pollutant, have been clarified to induce testicular disorder in mammals. And the current studies have delineated a correlation between gut microbiota and male reproduction. However, it's still unclear whether gut microbiota gets involved in MPs-induced reproductive toxicity. In this work, we constructed a mouse model drinking 5 μm polystyrene-MPs (PS-MPs) at the concentrations of 100 μg/L and 1000 μg/L for 90 days. Evident histological damage, spermatogenetic disorder and hormones synthesis inhibition were observed in PS-MPs exposed mice. With fecal microbiota transplantation (FMT) trial, the recipient mice exhibited gut microbial alteration, and the elevated abundance of Bacteroides and Prevotellaceae_UCG-001 were positively correlated with testicular disorder according to spearman correlation analysis. Mechanistically, increased proportion of pro-inflammatory bacteria may drive translocation of T helper 17 (Th17) cells, resulting in overproduced interleukin (IL)-17 A and downstream inflammatory response in both the mice exposed to PS-MPs and corresponding recipient mice. In summary, our findings revealed the critical role of gut microbiota in PS-MPs-induced reproductive toxicity, and tried to elucidate the underlying mechanism of gut microbial dysregulation-mediated IL-17 A signaling pathway. Furthermore, this study also provides the research basis for gut microbiota-targeted treatment of male infertility in the future.

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          Most cited references61

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          Accumulation of microplastic on shorelines woldwide: sources and sinks.

          Plastic debris 1900 fibers per wash. This suggests that a large proportion of microplastic fibers found in the marine environment may be derived from sewage as a consequence of washing of clothes. As the human population grows and people use more synthetic textiles, contamination of habitats and animals by microplastic is likely to increase.
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            Human Consumption of Microplastics

            Microplastics are ubiquitous across ecosystems, yet the exposure risk to humans is unresolved. Focusing on the American diet, we evaluated the number of microplastic particles in commonly consumed foods in relation to their recommended daily intake. The potential for microplastic inhalation and how the source of drinking water may affect microplastic consumption were also explored. Our analysis used 402 data points from 26 studies, which represents over 3600 processed samples. Evaluating approximately 15% of Americans' caloric intake, we estimate that annual microplastics consumption ranges from 39000 to 52000 particles depending on age and sex. These estimates increase to 74000 and 121000 when inhalation is considered. Additionally, individuals who meet their recommended water intake through only bottled sources may be ingesting an additional 90000 microplastics annually, compared to 4000 microplastics for those who consume only tap water. These estimates are subject to large amounts of variation; however, given methodological and data limitations, these values are likely underestimates.
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              The gut-liver axis in liver disease: pathophysiological basis for therapy

              The gut-liver axis refers to the bidirectional relationship between the gut and its microbiota, and the liver, resulting from the integration of signals generated by dietary, genetic and environmental factors. This reciprocal interaction is established by the portal vein which enables transport of gut-derived products directly to the liver, and the liver feedback route of bile and antibody secretion to the intestine. The intestinal mucosal and vascular barrier is the functional and anatomical structure that serves as a playground for the interactions between the gut and the liver, limiting the systemic dissemination of microbes and toxins while allowing nutrients to access the circulation and to reach the liver. The control of microbial communities is critical to maintaining homeostasis of the gut-liver axis, and as part of this bidirectional communication the liver shapes intestinal microbial communities. Alcohol disrupts the gut-liver axis at multiple interconnected levels, including the gut microbiome, mucus barrier, epithelial barrier and at the level of antimicrobial peptide production, which increases microbial exposure and the proinflammatory environment of the liver. Growing evidence indicates the pathogenetic role of microbe-derived metabolites, such as trimethylamine, secondary bile acids, short-chain fatty acids and ethanol, in the pathogenesis of non-alcoholic fatty liver disease. Cirrhosis by itself is associated with profound alterations in gut microbiota and damage at the different levels of defence of the intestinal barrier, including the epithelial, vascular and immune barriers. The relevance of the severe disturbance of the intestinal barrier in cirrhosis has been linked to translocation of live bacteria, bacterial infections and disease progression. The identification of the elements of the gut-liver axis primarily damaged in each chronic liver disease offers possibilities for intervention. Beyond antibiotics, upcoming therapies centred on the gut include new generations of probiotics, bacterial metabolites (postbiotics), faecal microbial transplantation, and carbon nanoparticles. FXR-agonists target both the gut and the liver and are currently being tested in different liver diseases. Finally, synthetic biotic medicines, phages that target specific bacteria or therapies that create physical barriers between the gut and the liver offer new therapeutic approaches.
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                Author and article information

                Contributors
                Journal
                Environmental Pollution
                Environmental Pollution
                Elsevier BV
                02697491
                September 2022
                September 2022
                : 309
                : 119789
                Article
                10.1016/j.envpol.2022.119789
                35843456
                4cd3e75a-cc3c-4520-98f7-e99fc77c6a14
                © 2022

                https://www.elsevier.com/tdm/userlicense/1.0/

                https://doi.org/10.15223/policy-017

                https://doi.org/10.15223/policy-037

                https://doi.org/10.15223/policy-012

                https://doi.org/10.15223/policy-029

                https://doi.org/10.15223/policy-004

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