Paraquat, a widely used herbicide, causes environmental pollution, and liver injury in humans and animals. As a natural compound in fruits, ellagic acid (EA) shows anti-inflammatory and antioxidant effects. This study examines the beneficial effects of dietary EA against the paraquat-induced hepatic injury and further explores the underlying molecular mechanisms using a piglet model. Post-weaning piglets are fed basal diet supplemented with 50 mg/kg, 100 mg/kg, or 200 mg/kg EA for 3 weeks. At week 2, hepatic injury is induced by 4 mg/kg paraquat followed by 7 days recovery. EA supplementation significantly mitigates paraquat-induced hepatic fibrosis, steatosis, and high apoptotic rate. In agreement, EA supplementation reduces serum pro-inflammatory levels, ameliorates inflammatory cells infiltration into hepatic tissue, which are associated with suppressed NF-κB signaling during paraquat exposure. In addition, EA supplementation significantly improves activities of antioxidative enzymes which were correlated with activated Nrf2/Keap 1 signaling during paraquat exposure. Furthermore, EA supplementation restores cecal microbial community during paraquat exposure. The protective effect of EA is strongly linked with increased relative abundance of Lactobacillus reuteri and Lactobacillus amylovorus. Taken together, EA supplementation effectively reduced the occurrence of hepatic oxidative damage and inflammation induced by paraquat through modulating cecal microbial communities, which provides a novel nutritional therapeutic strategy for hepatic injury.

In recent years, pollution of antibiotics and heavy metal has often been reported in organic wastes. Saprophytic insects have been recorded as biological control agents in organic waste management. During organic waste conversion, the intestinal bacteria of the saprophytic insects play an important role in digestion, physiology, immunity and prevention of pathogen colonization. Black soldier fly (BSF) Hermetia illucens has been widely used as saprophytic insects and showed tolerance to sulfonamides (SAs) and cadmium (Cd). Diversity and changes in gut microbiota of black soldier fly larvae (BSFL) were evaluated through 16S rRNA high-throughput sequencing, and a decrease in diversity of gut microbiota along with an increase in SAs stress was recorded. Major members identified were Actinomycetaceae, Enterobacteriaceae, and Enterococcaceae. And fourteen multi-resistance Klebsiella pneumoniae strains were isolated. Two strains BSFL7-B-5 (from middle midgut of 7-day BSFL) and BSFL11-C-1 (from posterior midgut of 11-day BSFL) were found to be low-toxic and multi-resistance. The adsorption rate of SAs in 5 mg/kg solutions by these two strains reached 65.2% and 61.6%, respectively. Adsorption rate of Cd in 20 mg/L solutions was 77.2% for BSFL7-B-5. The strain BSFL11-C-1 showed higher than 70% adsorption rates of Cd in 20, 30 and 40 mg/L solutions. This study revealed that the presence of multi-resistance bacterial strains in the gut of BSFL helped the larvae against SAs or Cd stress. After determining how and where they are used, selected BSFL gut bacterial strains might be utilized in managing SAs or Cd contamination at suitable concentrations in the future.

Microplastics (MPs) have become an emerging threat for organisms. However, the toxicity mechanisms on biota, especially soil biota remain largely unclear. This study distinguished the effects of five types of MPs and their extractable additives on a typical soil oligochaete Enchytraeus crypticus using a traditional ecotoxicological approach combined with gut microbiota analysis. A variety of inorganic and organic compounds were screened in extractable solutions. Both MPs and their extractable additives decreased the growth and survival rates of the worms and shifted the gut microbiota, and the effects were type-specific. The differences between the effects of MPs and their extractable additives on traditional ecotoxicological parameters were insignificant, suggesting that extractable additives were the main toxicity pathways on soil fauna. The type-specific effects of MPs were attributed to the varied chemical compositions of extractable additives, and the compounds responsible for the shift of gut microbiota were further identified. The distinguishable effects on gut microbiota between MPs and their extractable additives together with the significant regressions between gut microbiota and traditional ecotoxicological parameters confirmed that gut microbiota could be a more sensitive indicator of organism's health conditions. Combined, the study provided an important insight into the toxicity mechanisms of MPs on soil fauna and extractable additives of MPs may be a hidden threat.

The intestine is not only the main accumulation organ of microplastics (MPs), but also the intestinal environment is very conductive to the release of additives in MPs. However, the kinetics of release process, influence factors, and the related effects on gut microbiota remain largely unknown. In this study, a mucosal-simulator of the human intestinal microbial ecosystem (M-SHIME) was used to investigate the influence of gut microbiota on the release of phthalates (PAEs) from MPs and the effects of MPs on the intestinal luminal microbiota and mucosal microbiota. We found that di-(2-ethylhexyl) phthalate (DEHP), di-n-butyl phthalate (DBP), and dimethyl phthalate (DMP) were the dominant PAEs released in the gut. Gut microbiota accelerated the release of PAEs, with the time to reach the maximum release was shortened from 7 days to 2 days. Moreover, MPs induced differential effects on luminal microbiota and mucosal microbiota. Compared with mucosal microbiota, the luminal microbiota was more susceptible to the leaching of PAEs from MPs, as evidenced by more microbiota alterations. MPs also inhibited the metabolic activity of intestinal flora based on the reduced production of short chain fatty acids (SCFA). These effects were mainly contributed by the release of PAEs. Acidaminococcus and Morganella were simultaneously correlated to the release of PAEs and the inhibition of metabolic activity of intestinal microbiota and can be used as indicators for the intestinal exposure of MPs and additives.

Perfluorooctanesulfonic acid (PFOS) is a persistent anthropogenic chemical that can affect the thyroid hormone system in humans and animals. In adults, thyroid hormones (THs) are regulated by the hypothalamic-pituitary-thyroid (HPT) axis, but also by organs such as the liver and potentially the gut microbiota. PFOS and other xenobiotics can therefore disrupt the TH system at various locations and through different mechanisms. To start addressing this, we exposed adult male rats to 3 mg PFOS/kg/day for 7 days and analysed effects on multiple organs and pathways simultaneously by transcriptomics. This included four primary organs involved in TH regulation, namely hypothalamus, pituitary, thyroid, and liver. To investigate a potential role of the gut microbiota in thyroid hormone regulation, two additional groups of animals were dosed with the antibiotic vancomycin (8 mg/kg/day), either with or without PFOS. PFOS exposure decreased thyroxine (T4) and triiodothyronine (T3) without affecting thyroid stimulating hormone (TSH), resembling a state of hypothyroxinemia. PFOS exposure resulted in 50 differentially expressed genes (DEGs) in the hypothalamus, 68 DEGs in the pituitary, 71 DEGs in the thyroid, and 181 DEGs in the liver. A concomitant compromised gut microbiota did not significantly change effects of PFOS exposure. Organ-specific DEGs did not align with TH regulating genes; however, genes associated with vesicle transport and neuronal signaling were affected in the hypothalamus, and phase I and phase II metabolism in the liver. This suggests that a decrease in systemic TH levels may activate the expression of factors altering trafficking, metabolism and excretion of TH. At the transcriptional level, little evidence suggests that the pituitary or thyroid gland is involved in PFOS-induced TH system disruption.

Nanoplastic is recognized as an emerging environmental pollutant due to the anticipated ubiquitous distribution, increasing concentration in the ocean, and potential adverse health effects. While our understanding of the ecological impacts of nanoplastics is still limited, we benefit from relatively rich toxicological studies on other nanoparticles such as nano metal oxides. However, the similarity and difference in the toxicokinetic and toxicodynamic aspects of plastic and metallic nanoparticles remain largely unknown. In this study, juvenile Pacific white shrimp Litopenaeus vannamei was exposed to two types of nanoparticles at environmentally relative low and high concentrations, i.e., 100 nm polystyrene nanoplastics (nano-PS) and titanium dioxide nanoparticles (nano-TiO₂) via dietary exposure for 28 days. The systematic toxicological evaluation aimed to quantitatively compare the accumulation, excretion, and toxic effects of nano-PS and nano-TiO₂. Our results demonstrated that both nanoparticles were ingested by L. vannamei with lower egestion of nano-TiO₂ than nano-PS. Both nanoparticles inhibited the growth of shrimps, damaged tissue structures of the intestine and hepatopancreas, disrupted expression of immune-related genes, and induced intestinal microbiota dysbiosis. Nano-PS exposure caused proliferative cells in the intestinal tissue, and the disturbance to the intestinal microbes was also more serious than that of nano-TiO₂. The results indicated that the effect of nano-PS on the intestinal tissue of L. vannamei was more severe than that of nano-TiO₂ with the same particle size. The study provides new theoretical basis of the similarity and differences of their toxicity, and highlights the current lack of knowledge on various aspects of absorption, distribution, metabolism, and excretion (ADME) pathways of nanoplastics.

Plastic ingestion has been widely investigated to understand its adverse harms on fauna, but the role of fauna itself in plastic fragmentation has been rarely addressed. Here, we review and discuss the available experimental results on the role of terrestrial and aquatic macrofauna in plastic biofragmentation and degradation. Recent studies have shown how biting, chewing, and stomach contractions of organisms shatter ingested plastic along their digestive tracts. Gut microbial communities can play a role in biodegradation and their composition can shift according to the type of plastic ingested. Shifts in molecular weights, chemical bond forming and breaking, and changes in thermal modification detected in the plastic debris present in the faeces also suggest active biodegradation. A few studies have also shown interactions other than ingestion, such as burrowing, may actively or passively promote physical plastic fragmentation by fauna. We suggest that further investigations into the role of fauna in physical fragmentation and chemical degradation linked to active ingestion and gut associated microbiota metabolism, respectively, should be conducted to better evaluate the impact of these mechanisms on the release of micro- and nano-plastic in the environment. Knowledge on macrofauna other than marine invertebrates and terrestrial soil dwelling invertebrates is particularly lacking, as well as focus on broader types of plastic polymers.

Antibiotics are omnipresent in the environment due to their widespread use, and they have wide-ranging negative impacts on organisms. Virus resistance differs substantially between domesticated Apis mellifera and wild Apis cerana, although both are commonly raised in China. Here, we investigated whether antibiotics can increase the sensitivity of honey bees to viral infection using the Israeli acute paralysis virus (IAPV) and tetracycline as representative virus and antibiotic. Although IAPV multiplied to lower levels in A. cerana than A. mellifera, resulting in decreased mortality (P < 0.01), there was no significant difference in immune responses to viral infection between the two species. Adult worker bees (A. cerana and A. mellifera) were treated with or without tetracycline to demonstrate the prominent role of gut microbiota against viral infection, and found Lactobacillus played a vital antiviral role in A. cerana. In A. cerana but not A. mellifera, tetracycline treatment reduced clearly bee survival and increased susceptibility to IAPV infection (P < 0.01). Our findings revealed that long-term antibiotic treatment in A. mellifera had altered the native gut microbiome and promoted the sensitivity to viral infection. We highlight the effects of antibiotics exposure on resistance to microbial and viral infection.

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.

The microbiome has been described as an additional host “organ” with well-established beneficial roles. However, the effects of exposures to chemicals on both structure and function of the gut microbiome of fishes are understudied. To determine effects of benzo[a]pyrene (BaP), a model persistent organic pollutant, on structural shifts of gut microbiome in juvenile fathead minnows (Pimephales promelas), fish were exposed ad libitum in the diet to concentrations of 1, 10, 100, or 1000 μg BaP g⁻¹ food, in addition to a vehicle control, for two weeks. To determine the link between exposure to BaP and changes in the microbial community, concentrations of metabolites of BaP were measured in fish bile and 16S rRNA amplicon sequencing was used to evaluate the microbiome. Exposure to BaP only reduced alpha-diversity at the greatest exposure concentrations. However, it did alter community composition assessed as differential abundance of taxa and reduced network complexity of the microbial community in all exposure groups. Results presented here illustrate that environmentally-relevant concentrations of BaP can alter the diversity of the gut microbiome and community network connectivity.