Plastics have become an integral part of our daily lives. In the environment, plastics break down into small pieces (<5 mm) that are referred to as microplastics. Microplastics are ubiquitous and widespread in the environment, and all living organisms are exposed to their effects. The present study provides new insights into the potential effects of polyethylene terephthalate (PET) microplastics on organisms via extracellular vesicle (EV)-mediated communication. The study demonstrated that serum-derived EVs are able to transport plastic particles. In addition, PET microplastics alter the content of miRNA in EVs. The identified differentially regulated miRNAs may target genes associated with lifestyle diseases, such as cardiovascular or metabolic diseases, and carcinogenesis. This work expands our understanding of PET microplastics' effects on organisms via EV-mediated communication and identifies directions for further research and strategies.

Microplastics are a widespread environmental hazard and their impact on human health has become a growing concern in last years. Recently, the potential role of microplastics in the development of various diseases, including diabetes, has been highlighted. Therefore, the aim of this study was to investigate the effects of PET microplastics on the pancreas using immature pigs as a model organism. We analyzed the global transcriptomic profile of the pancreas by RNA-Seq in piglets treated with either a low (0.1 g/day) or a high dose (1 g/day) of PET microplastics for 4 weeks. The analysis revealed a dose-dependent effect of PET microplastics on gene expression. A low dose changed the expression of one gene, while a high dose affected the expression of 86 genes. The differentially expressed genes, including immune cell markers, cytokines and chemokines, may activate the immune system in the pancreas in a way that is characteristic of the pathogenesis of diabetes. In addition, PET microplastics induced oxidative stress in the pancreas. These above imply that oral exposure to PET microplastics could be a new risk factor for the development of diabetes.

Inflammation in the female reproductive system causes serious health problems including infertility. The aim of this study was to determine the in vitro effects of peroxisome proliferator-activated receptor-beta/delta (PPARβ/δ) ligands on the transcriptomic profile of the lipopolysaccharide (LPS)-stimulated pig corpus luteum (CL) in the mid-luteal phase of the estrous cycle using RNA-seq technology. The CL slices were incubated in the presence of LPS or in combination with LPS and the PPARβ/δ agonist—GW0724 (1 μmol/L or 10 μmol/L) or the antagonist—GSK3787 (25 μmol/L). We identified 117 differentially expressed genes after treatment with LPS; 102 and 97 differentially expressed genes after treatment, respectively, with the PPARβ/δ agonist at a concentration of 1 μmol/L or 10 μmol/L, as well as 88 after the treatment with the PPARβ/δ antagonist. In addition, biochemical analyses of oxidative status were performed (total antioxidant capacity and activity of peroxidase, catalase, superoxide dismutase, and glutathione S-transferase). This study revealed that PPARβ/δ agonists regulate genes involved in the inflammatory response in a dose-dependent manner. The results indicate that the lower dose of GW0724 showed an anti-inflammatory character, while the higher dose seems to be pro-inflammatory. We propose that GW0724 should be considered for further research to alleviate chronic inflammation (at the lower dose) or to support the natural immune response against pathogens (at the higher dose) in the inflamed corpus luteum.

Extracellular vesicles (EVs) are essential mediators of intercellular communication. They play a crucial role in maintaining homeostasis, regulating physiological processes and contribute to the development of various diseases. Microplastics can enter the human body as ubiquitous pollutants and have been detected in various tissues. In the body, they can disrupt physiological functions, leading to increasing health concerns. However, their impact on EV-mediated communication remains poorly understood. Therefore, the aim of this study was to determine whether PET microplastics - one of the most used materials in plastic packaging - affect the content of EVs using immature pigs as a model organism. The global metabolomic profile of serum-derived EVs was analyzed by UPLC-MS in piglets treated with either a low (0.1 g/day) or a high dose (1 g/day) of PET microplastics for 4 weeks. The analysis showed that a low dose affected the expression of 24 metabolites, while a high dose affected the expression of 31 metabolites. The differentially expressed metabolites were involved in the regulation of lipid signaling pathways, mitochondrial dysfunction, disruption of glucose metabolism and impaired steroidogenesis. The results of these studies reveal a new pathway of communication in the body in response to PET microplastics.

Helminths are masters at manipulating host's immune response. Especially, parasitic nematodes have evolved strategies that allow them to evade, suppress, or modulate host's immune response to persist and spread in the host's organism. While the immunomodulatory effects of nematodes on their hosts are studied with a great commitment, very little is known about nematodes' own immune system, immune response to their pathogens, and interactions between parasites and bacteria in the host's organism. To illustrate the response of the parasitic nematode Anisakis simplex s.s. during simulated interaction with Escherichia coli, different concentrations of lipopolysaccharide (LPS) were used, and the proteomic analysis with isobaric mass tags for relative and absolute quantification (tandem mass tag–based LC–MS/MS) was performed. In addition, gene expression and biochemical analyses of selected markers of oxidative stress were determined. The results revealed 1148 proteins in a group of which 115 were identified as differentially regulated proteins, for example, peroxiredoxin, thioredoxin, and macrophage migration inhibitory factor. Gene Ontology annotation and Reactome pathway analysis indicated that metabolic pathways related to catalytic activity, oxidation–reduction processes, antioxidant activity, response to stress, and innate immune system were the most common, in which differentially regulated proteins were involved. Further biochemical analyses let us confirm that the LPS induced the oxidative stress response, which plays a key role in the innate immunity of parasitic nematodes. Our findings, to our knowledge, indicate for the first time, the complexity of the interaction of parasitic nematode, A. simplex s.s. with bacterial LPS, which mimics the coexistence of helminth and gut bacteria in the host. The simulation of this crosstalk led us to conclude that the obtained results could be hugely valuable in the integrated systems biology approach to describe a relationship between parasite, host, and its commensal bacteria.