An unhealthy diet has been linked to increased incidence of chronic diseases. To investigate the relationship between diet and intestinal inflammation, mice in two experimental groups were fed on a high-fat diet or high-fructose diet, respectively. The result showed that the defecation volume of the experimental groups was significantly reduced compared with that of the control group, and the levels of pro-inflammatory cytokines (interleukin (IL)-1β and IL-6) and IgG in serum were increased significantly. In addition, inflammatory cell infiltration was observed in intestinal tissue, indicating that a high-fructose or high-fat diet can lead to constipation and inflammation. Further analysis showed that the microbial composition of the experimental groups changed significantly, including a decrease of the Bacteroidetes/Firmicutes ratio and increased levels of Bacteroides, Akkermansia, Lactobacillus, and Ruminococcus, which might be associated with inflammation. The results of pro-inflammatory metabolites analysis showed that the levels of arachidonic acid, stearic acid, and indoxylsulfuric acid were significantly increased in the experimental groups, which were related significantly to Bacteroides, Enterococcus, and Akkermansia. Meanwhile, the content of 5-hydroxytryptamine (5-HT) was significantly decreased, which might cause constipation by reducing intestinal peristalsis. Moreover, transplantation of fecal bacteria from inflammatory mice caused constipation and inflammation in normal mice, which could be relieved by feeding a normal diet. The results of the present study indicated that changes in intestinal microbiota and microbial metabolites may underlie chronic intestinal inflammation and constipation caused by high-fructose and high-fat diets.

Diet can not only provide nutrition for intestinal microbiota, it can also remodel them. However, is unclear whether and how diet affects the spread of antibiotic resistance genes (ARGs) in the intestinal microbiota. Therefore, we employed selected high-sugar, high-fat, high-protein, and normal diets to explore the effect. The results showed that high-sugar, high-fat, and high-protein diets promoted the amplification and transfer of exogenous ARGs among intestinal microbiota, and up-regulated the expression of trfAp and trbBp while significantly altered the intestinal microbiota and its metabolites. Inflammation-related products were strongly correlated with the spread of ARGs, suggesting the intestinal microenvironment after diet remodeling might be conducive to the spreading of ARGs. This may be attributed to changes in bacterial membrane permeability, the SOS response, and bacterial composition and diversity caused by diet-induced inflammation. In addition, acceptor bacteria (zygotes) screened by flow cytometry were mostly Proteobacteria, Firmicutes and Actinobacteria, and most were derived from dominant intestinal bacteria remodeled by diet, indicating that the transfer of ARGs was closely linked to diet, and had some selectivity. Metagenomic results showed that the gut resistance genome could be affected not only by diet, but by exogenous antibiotic resistant bacteria (ARB). Many ARG markers coincided with bacterial markers in diet groups. Therefore, dominant bacteria in different diets are important hosts of ARGs in specific dietary environments, but the many pathogenic bacteria present may cause serious harm to human health.

Antibiotic failure is occurring worldwide. In a routine surveillance study on antibioticresistance genes (ARGs) in natural water bodies, we noted the detection of colistin-resistance gene mcr-1, previously identified in Escherichia coli and Klebsiella pneumoniae isolates from human beings and animals in several countries. The mcr-1 gene might be present in water environments, because aquatic ecosystems are recognized as reservoirs for antibiotic resistant bacteria (ARB) and ARGs. In this study, a qPCR assay was developed to monitor and quantify the mcr-1 gene in the Haihe River, China. The results showed that all 18 samples collected from different locations over 6 months along the Haihe River were positive for the mcr-1 gene, and the highest level of mcr-1 reached 3.81 × 105 gene copies (GC) per liter of water. This is the first study to quantify mcr-1 in a natural water system by qPCR. Our findings highlight the potential for this antibiotic resistance determinant to spread extensively, suggesting a significant health and ecological impact.

While nanoparticles exert bactericidal effects through the generation of reactive oxygen species (ROS), the processes of the internalization of and the direct physical damage caused by iron oxide nanoparticles are not completely clear. We hypothesize that direct physical or mechanical damage of the cell membrane and cytoplasmic integrity by nanoparticles is another major cause of bacterial death besides ROS. The aim of this study is to investigate the process of the internalization of iron oxide nanoparticles, and to evaluate the effect of direct physical or mechanical damage on bacterial cell growth and death. The results demonstrate that iron oxide nanoparticles not only inhibited E. coli cell growth, but also caused bacterial cell death. Iron oxide nanoparticles produced significantly elevated ROS levels in bacteria. Transmission electronic microscopy demonstrated that iron oxide nanoparticles were internalized into and condensed the cytoplasm. Strikingly, we observed that the internalized nanoparticles caused intracellular vacuole formation, instead of simply adsorbing thereon; and formed clusters on the bacterial surface and tore up the outer cell membrane to release cytoplasm. This is the first time that the exact process of the internalization of iron oxide nanoparticles has been observed. We speculate that the intracellular vacuole formation and direct physical or mechanical damage caused by the iron oxide nanoparticles caused the bactericidal effect, along with the effects of ROS.

The latent dangers of waterborne viral transmission have become a major public health concern. In this study, reduced graphene oxide (rGO)-Fe₃O₄ nanoparticles were decorated with cetyltrimethylammonium bromide (CTAB) to adsorb severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) spike pseudovirus and three human enteric viruses (HuNoV, HRV, and HAdV). The successful combination of CTAB with rGO-Fe₃O₄ was confirmed by transmission electron microscopy, X-ray diffraction, Fourier-transform infrared spectroscopy, zeta potential, Brunner-Emmet-Teller, and vibrating sample magnetometer measurements. The adsorption of HuNoV and HAdV followed pseudo-first-order kinetics, while that of HRV conformed to the pseudo-second-order model. CTAB-functionalized rGO-Fe₃O₄ exhibited exceptionally high adsorption of HuNoV, HRV, HAdV and SARS-CoV-2 spike pseudovirus, with maximum adsorption capacities of 3.55 × 10⁷, 7.01 × 10⁷, 2.21 × 10⁷ and 6.92 × 10⁶ genome copies mg⁻¹, respectively. Moreover, the composite could effectively adsorb the four types of virus particles from coastal, tap, and river water. In addition, concentrating the virions using CTAB functionalized rGO-Fe₃O₄ composites before qPCR analysis significantly improved the detection limit. The results indicate that viruses are captured on the surface of CTAB functionalized rGO-Fe₃O₄ composites through electrostatic interactions and the intrinsic adsorption ability of rGO. Overall, CTAB-functionalized rGO-Fe₃O₄ composites are promising materials for the adsorption and detection of human enteric viruses as well as SARS-CoV-2 from complex aqueous environments.