Antibiotics, antimicrobial resistance determinants and human pathogens are new types of environmental pollutants that pose a great threat to human health. Wastewater treatment plants (WWTPs) are important sources of novel pollutants; however, few studies have investigated their impact on surrounding natural water. Therefore, this study used a WWTP as the entry point to explore WWTP removal efficiency of antibiotics, antimicrobial resistance determinants and human pathogens and further analyze the impact of WWTP effluent on receiving waters. The investigated WWTP had a good removal effect on fluoroquinolones, macrolides, lincomycin, sulfanilamide, tetracycline and chloramphenicol antibiotics in wastewater, and the concentration of antibiotics in the WWTP's effluent was reduced by >80% relative to the influent. In addition to cmlA, the effect of the WWTP on antimicrobial resistance determinants removal was poor, although the effluent from the WWTP had no effect on the abundance of antimicrobial resistance determinants in the receiving water. However, with the dilution of receiving water, the abundance of antimicrobial resistance determinants gradually decreased. The WWTP could reduce the abundance of bacteria by 1000 times from influent water to effluent water. The major bacteria in the influent and effluent were Bacteroidetes and Proteobacteria. After effluent is discharged into receiving water, Cyanobacteria proliferate in large quantities, which can affect the microbial structure in the environment.The abundance of Acinetobacter, which was the predominant potential human pathogen in local wastewater, decreased dramatically after wastewater treatment. We also conducted an ecological risk assessment of the antibiotics identified and found that the ecological risk AZM and CLR posed to aquatic organisms was high. Overall, we identified the efficiency of WWTP control of antibiotics, antimicrobial resistance determinants and potential human pathogens and the impact of WWTP effluent on receiving water and provided data to support the control of the investigated pollutants.

Objective: This study aims to analyze the changes of fecal short chain fatty acids (SCFAs) content and gut microbiota composition in sepsis associated encephalopathy (SAE) mice, further evaluating the effect of SCFAs on cognitive function and the underlying mechanism in SAE mice.Methods: A total of 55 male adult C57BL/6 mice (2–3 months of age, 20–25 g) were divided into four groups randomly: sham group (n = 10), cecal ligation and puncture group (CLP group, n = 15), CLP+SCFAs group (n = 15), and CLP+SCFAs+GLPG0974 group (n = 15). Seven days after surgery, fecal samples were collected for microbiota composition and SCFA analysis from 6 mice in each group randomly. Behavioral test was applied to assess cognitive impairment at the same time. After that, mice were sacrificed and brain tissue was harvested for inflammatory cytokines analysis.Results: The levels of acetic acid (.57 ± 0.09 vs 2.00 ± 0.24, p < 0.001) and propionic acid (.32 ± 0.06 vs .66 ± 0.12, p = 0.002) were significantly decreased in the CLP group compared with the sham group. The administration of SCFAs significantly increased the levels of acetic acid (1.51 ± 0.12 vs. 0.57 ± 0.09, p < 0.001) and propionic acid (0.54 ± 0.03 vs. 0.32 ± 0.06, p = 0.033) in CLP+SCFAs group compared with CLP group. Relative abundance of SCFAs-producing bacteria, including Allobaculum (0.16 ± 0.14 vs. 15.21 ± 8.12, p = 0.037), Bacteroides (1.82 ± 0.38 vs. 15.21 ± 5.95, p = 0.002) and Bifidobacterium (0.16 ± 0.06 vs. 2.24 ± 0.48, p = 0.002), significantly decreased in the CLP group compared with the sham group. The behavioral tests suggested that cognitive function was impaired in SAE mice, which could be alleviated by SCFAs pretreatment. ELISA tests indicated that the levels of IL-1β, IL-6, and TNF-α were elevated in SAE mice and SCFAs could lower them. However, the GPR43 antagonist, GLPG0974, could reverse the cognitive protective effect and anti-neuroinflammation effect of SCFAs.Conclusion: Our study suggested that in SAE, the levels of acetate and propionate decreased significantly, accompanied by gut microbiota dysbiosis, particularly a decrease in SCFAs-producing bacteria. GPR43 was essential for the anti-neuroinflammation and cognitive protective effect of SCFAs in SAE.