Bacteria are candidates for the biotransformation of environmental arsenic (As), while As metabolism in bacteria is not yet fully understood. In this study, we sequenced the genome of an As-resistant bacterium strain Stenotrophomonas maltophilia SCSIOOM isolated from the fish gut. After arsenate (As(V)) exposure, S. maltophilia transformed As(V) to organoarsenicals, along with the significant change of the expression of 40 genes, including the upregulation of arsH, arsRBC and betIBA. The heterogeneous expression of arsH and arsRBC increased As resistance of E. coli AW3110 by increasing As efflux and transformation. E. coli AW3110 (pET-betIBA) could transform inorganic As into dimethylarsinate (DMA) and nontoxic arsenobetaine (AsB), which suggested that AsB could be synthesized through the synthetic pathway of its analog-glycine betaine. In addition, the existence of arsRBC, betIBA and arsH reduced the reactive oxygen species (ROS) induced by As exposure. In total, these results demonstrated that S. maltophilia adopted an As metabolism strategy by reducing As accumulation and synthesizing less toxic As species. We first reported the production and potential synthetic pathway of AsB in bacteria, which improved our knowledge of As toxicology in microorganisms.

The prevalence and transmission of antibiotic resistance genes (ARGs) and opportunistic pathogens in water environments can pose great threat to public health. However, the dissemination of ARGs and opportunistic pathogens from water environments to humans has been poorly explored. Here, we employed 16S rRNA gene sequencing and high-throughput quantitative PCR techniques to explore the seasonal distribution of ARGs and opportunistic pathogens in the Yellow River water (source water) and tap water, as well as their relationships with healthy humans at Lanzhou, China. Physiochemical analysis was applied to detect water quality parameters and heavy metal contents. The absolute abundance and diversity of ARGs in the Yellow River and tap water demonstrated distinct seasonal patterns. In winter, the Yellow river water had the highest ARG abundance and diversity, while tap water owned the lowest. Mobile genetic elements (MGEs) were the predominant driver of ARG profiles in both the Yellow river and tap water. Null model analysis showed that ARG assembly in the Yellow River was more influenced by stochastic processes than tap water and this was independent of seasons. Total organic carbon and arsenic contents exhibited positive correlations with many ARGs. Opportunistic pathogens Aeromonas and Pseudomonas may be potential hosts for ARGs. Approximately 80% of detected ARGs were shared between water samples and the human gut. These persistent ARGs could not be entirely eliminated through drinking water treatment processes. Thus, it is crucial to protect sources of tap water from anthropogenic pollution and improve water treatment technologies to reduce the dissemination of ARGs and ensure drinking-water biosafety for human health.

Antibiotic resistance genes (ARGs) are emerging contaminants that pose a potential risk to human health worldwide. In this study, a metagenomic analysis was performed to investigate the distribution of ARGs in paddy field ecosystems, crayfish monoculture pond ecosystems, and rice-crayfish cultivation field ecosystems. The results showed that MacB and BcrA are two dominant ARGs, and macrolide is the dominant antibiotic not only in the water, but also in the sediment and gut of crayfish, in both the crayfish monoculture and the rice-crayfish cultivation ecosystems. Meanwhile, some lower-abundance ARGs in the water and sediment of crayfish cultivation ecosystems were significantly different in their abundance than those in rice paddy fields, and the ARGs in crayfish culture system and rice paddy fields showed even higher dissimilarities of diversity. Comprehensive analysis with redundancy analysis（RDA）and the distribution of dominant ARGs showed that the dissimilarity was related to the higher concentrations of total nitrogen (TN), total phosphorus (TP), chlorophyll a (Chla), permanganate index (CODMₙ₎, and nitrate in the water of rice paddy fields, and was related to the higher contents of N, P, K, and organic matter (OM) in the sediment of rice paddy fields. The source trackers of ARGs within the crayfish cultivation ponds and the rice-crayfish cultivation fields showed that the sediment in crayfish cultivation ponds mainly played the role of the ‘sink’ for ARGs, and the water and gut of crayfish mutually contributed to the high rates of ARGs. The ARG contribution rates of crayfish gut and sediment decreased and increased, respectively, in rice-crayfish cultivation fields and in crayfish monoculture ponds, which might be related to the lower crayfish biomass and the lower water depth in rice-crayfish cultivation fields.

Mammalian polychlorinated biphenyl (PCB) metabolism has not been systematically explored with nontarget high-resolution mass spectrometry (Nt-HRMS). Here we investigated the importance of the gut microbiome in PCB biotransformation by Nt-HRMS analysis of feces from conventional (CV) and germ-free (GF) adult female mice exposed to a single oral dose of an environmental PCB mixture (6 mg/kg or 30 mg/kg in corn oil). Feces were collected for 24 h after PCB administration, PCB metabolites were extracted from pooled samples, and the extracts were analyzed by Nt-HRMS. Twelve classes of PCB metabolites were detected in the feces from CV mice, including PCB sulfates, hydroxylated PCB sulfates (OH-PCB sulfates), PCB sulfonates, and hydroxylated methyl sulfone PCBs (OH-MeSO₂-PCBs) reported previously. We also observed eight additional PCB metabolite classes that were tentatively identified as hydroxylated PCBs (OH-PCBs), dihydroxylated PCBs (DiOH-PCBs), monomethoxylated dihydroxylated PCBs (MeO-OH-PCBs), methoxylated PCB sulfates (MeO-PCB sulfates), mono-to tetra-hydroxylated PCB quinones ((OH)ₓ-quinones, x = 1–4), and hydroxylated polychlorinated benzofurans (OH-PCDF). Most metabolite classes were also detected in the feces from GF mice, except for MeO-OH-PCBs, OH-MeSO₂-PCBs, and OH-PCDFs. Semi-quantitative analyses demonstrate that relative PCB metabolite levels increased with increasing dose and were higher in CV than GF mice, except for PCB sulfates and MeO-PCB sulfates, which were higher in GF mice. These findings demonstrate that the gut microbiome plays a direct or indirect role in the absorption, distribution, metabolism, or excretion of PCB metabolites, which in turn may affect toxic outcomes following PCB exposure.

Mites are considered the worst enemy of honey bees, resulting in economic losses in agricultural production. In apiculture, flumethrin is frequently used to control mites. It causes residues of flumethrin in colonies which may threaten honey bees, especially for larvae. Still, the impact of flumethrin-induced dysbiosis on honey bees larval health has not been fully elucidated, and any impact of microbiota for decomposing flumethrin in honey bees is also poorly understood. In this study, 2-day-old larvae were fed with different flumethrin-sucrose solutions (0, 0.5, 5, 50 mg/kg) and the dose increased daily (1.5, 2, 2.5 and 3 μL) until capped, thereafter the expression level of two immune genes (hymenoptaecin, defensin1) and two detoxication-related genes (GST, catalase) were measured. Meanwhile, the effect of flumethrin on honey bee larvae (Apis mellifera) gut microbes was also explored via 16S rRNA Illumina deep sequencing. We found that flumethrin at 5 mg/kg triggered the over expression of immune-related genes in larvae, while the larval detoxification-related genes were up-regulated when the concentrations reached 50 mg/kg. Moreover, the abundance and diversity of microbes in flumethrin-treated groups (over 0.5 mg/kg) were significantly lower than control group, but it increased with flumethrin concentrations among the flumethrin-treated groups. Our results revealed that microbes served as a barrier in the honey bee gut and were able to protect honey bee larvae to a certain extent, and reduce the stress of flumethrin on honey bee larvae. In addition, as the concentration of flumethrin increases, honey bee larvae activate their immune system then detoxification system to defend against the potential threat of flumethrin. This is the first report on the impact of flumethrin on gut microbiota in honey bees larvae. The findings revealed new fundamental insights regarding immune and detoxification of host-associated microbiota.

Environmental health is increasingly compromised by persistent toxic substances, which may have serious implications in food safety and, thus, in human health. Polybrominated diphenyl ethers (PBDEs) are anthropogenic contaminants with endocrine disruption abilities and are commonly found in seafood, the main route of human exposure. Growing evidence points out that the human gut microbiota interacts with xenobiotics, which may lead to impairment of host homeostasis if functions of microbiota become compromised. The aim of this study was to ascertain if the physiological balance of human gut microbiome is affected by the presence and degree of exposure to PBDEs. Fermentation was performed in a batch closed-system using an inoculum made from fresh human stool. The volatolomic profile was analysed by solid-phase microextraction coupled to gas chromatography-mass spectrometry. Mesophilic, Gram-negative bacteria and coliforms were quantified by classic plating methods. Changes in the gut microbiome were evaluated after DNA extraction followed by deep sequencing of the 16S rDNA region. The exposure to PBDEs resulted in an imbalance in sulfur, short-chain fatty acids and aromatic organic compounds, changing the microbial volatolome in a dose- and time-dependent manner. Slight deviations in the microbial structure of human gut occurred in the presence of PBDEs, especially for high doses of exposure. For the first time, the impact of PBDEs on the microbial homeostasis of human gut microbiota was taken into consideration, revealing noteworthy modifications with serious health implications even at oral exposure doses considered as safe by worldwide regulatory entities.

Larvae of Zophobas atratus (synonym as Z. morio, or Z. rugipes Kirsch, Coleoptera: Tenebrionidae) are capable of eating foams of expanded polystyrene (EPS) and low-density polyethylene (LDPE), similar to larvae of Tenebrio molitor. We evaluated biodegradation of EPS and LDPE in the larvae from Guangzhou, China (strain G) and Marion, Illinois, U.S. (strain M) at 25 °C. Within 33 days, strain G larvae ingested respective LDPE and PS foams as their sole diet with respective consumption rates of 58.7 ± 1.8 mg and 61.5 ± 1.6 mg 100 larvae⁻¹d⁻¹. Meanwhile, strain M required co-diet (bran or cabbage) with respective consumption rates of 57.1 ± 2.5 mg and 30.3 ± 7.7 mg 100 larvae⁻¹ d⁻¹. Fourier transform infrared spectroscopy, proton nuclear magnetic resonance, and thermal gravimetric analyses indicated oxidation and biodegradation of LDPE and EPS in the two strains. Gel permeation chromatography analysis revealed that strain G performed broad depolymerization of EPS, i.e., both weight-average molecular weight (Mw) and number-average molecular weight (Mₙ) of residual polymers decreased, while strain M performed limited extent depolymerization, i.e., Mw and Mₙ increased. However, both strains performed limited extent depolymerization of LDPE. After feeding antibiotic gentamicin, gut microbes were suppressed, and Mw and Mₙ of residual LDPE and EPS in frass were basically unchanged, implying a dependence on gut microbes for depolymerization/biodegradation. Our discoveries indicate that gut microbe-dependent LDPE and EPS biodegradation is present within Z. atratus in Tenebrionidae, but that the limited extent depolymerization pattern resulted in undigested polymers with high molecular weights in egested frass.

The large accumulation of heavy metals in the soil surrounding steel factories has become a severe environmental problem. However, few studies have focused on how the earthworm gut microbiota responds to heavy metals in the soil. This study used research sites at a steel factory in Nanjing, China, to investigate how the soil bacterial community and earthworm gut microbiota respond differently to heavy metal contamination using Illumina high-throughput sequencing targeting 16S rRNA genes. The bacterial community of earthworm guts showed a distinct structure compared with that of the soil, featuring a higher relative abundance of Proteobacteria (45.7%) and Bacteroidetes (18.8%). The bacterial community in the earthworm gut appeared more susceptible to heavy metal contamination compared with the soil community. For example, we identified 38 OTUs (Operational taxonomic units) significantly influenced by contamination among 186 abundant OTUs in the soil, whereas 63 out of the 127 abundant OTUs in the earthworm gut were altered significantly under contamination. This susceptibility may be partly explained by the lower alpha diversity and distinct microbial interactions in the gut. In addition, the accumulation of heavy metals also stimulated the growth of potential plant growth promoting bacteria (PGPB) in the earthworm gut, especially those related to indole-3-acetic acid (IAA) and 1-aminocyclopropane-1-carboxylic acid deaminase (ACCD) production, which may potentially benefit the phyto-remediation of heavy metals. These results contribute to our understanding of the soil biota and its interactions under heavy metal contamination and may provide further insights into the phyto-remediation of metal-contaminated soil.

The usages of antibiotics in treating the pathogenic infections could alter the gut microbiome and associated resistome, causing long term adverse impact on human health. In this study, mice were treated with human-simulated regimen 25.0 mg kg⁻¹ of amoxicillin for seven days, and their gut microbiota and resistome were characterized using the 16S rRNA amplicons sequencing and the high-throughput qPCR, respectively. Meanwhile, the flora restorations after individual applications of inulin, Bifidobacterium longum (B. longum), and fecal microbiota transplantation (FMT) were analyzed for up to 35 days. The results revealed the prolonged negative impact of single course AMX exposure on mice gut microbiota and resistome. To be specific, pathobionts of Klebsiella and Escherichia-Shigella were significantly enriched, while prebiotics of Bifidobacterium and Lactobacillus were dramatically depleted. Furthermore, β-lactam resistance genes and efflux resistance genes were obviously enriched after amoxicillin exposure. Compared to B. longum, FMT and inulin were demonstrated to preferably restore the gut microbiota via reconstituting microbial community and stimulating specific prebiotic respectively. Such variation of microbiome caused their distinct alleviations on resistome alteration. Inulin earned the greatest elimination on AMX induced ARG abundance and diversity enrichment. FMT and B. longum caused remove of particular ARGs such as ndm-1, blaPER. Network analysis revealed that most of the ARGs were prone to be harbored by Firmicutes and Proteobacteria. In general, gut resistome shift was partly associated with the changing bacterial community structures and transposase and integron. Taken together, these results demonstrated the profound disruption of gut microbiota and resistome after single-course amoxicillin treatment and different restoration by inulin, B. longum and FMT.

Recently, environmental risk and toxicity of neonicotinoid insecticides to honey bees have attracted extensive attention. However, toxicological understanding of neonicotinoid insecticides on gut microbiota is limited. In the present study, honey bees (Apis mellifera L.) were exposed to a series of nitenpyram for 14 days. Results indicated that nitenpyram exposure decreased the survival and food consumption of honey bees. Furthermore, 16S rRNA gene sequencing revealed that nitenpyram caused significant alterations in the relative abundance of several key gut microbiotas, which contribute to metabolic homeostasis and immunity. Using high-throughput RNA-Seq transcriptomic analysis, we identified a total of 526 differentially expressed genes (DEGs) that were significantly altered between nitenpyram-treated and control honey bee gut, including several genes related to metabolic, detoxification and immunity. In addition, Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analysis showed nitenpyram affected several biological processes, of which most were related to metabolism. Collectively, our study demonstrates that the dysbiosis of gut microbiota in honey bee caused by nitenpyram may influence metabolic homeostasis and immunity of bees, and further decrease food consumption and survival of bees.