Cefotaxime Exposure-Caused Oxidative Stress, Intestinal Damage and Gut Microbial Disruption in Artemia sinica.

Cefotaxime (CTX) is an easily detectable antibiotic pollutant in the water environment, but little is known about its toxic effects on aquatic invertebrates, especially on the intestine. Here, we determined the oxidative stress conditions of A. sinica under CTX exposure with five concentrations (0, 0.001, 0.01, 0.1 and 1 mg/L) for 14 days. After that, we focused on changes in intestinal tissue morphology and gut microbiota in A. sinica caused by CTX exposure at 0.01 mg/L. We found malondialdehyde (MDA) was elevated in CTX treatment groups, suggesting the obvious antibiotic-induced oxidative stress. We also found CTX exposure at 0.01 mg/L decreased the villus height and muscularis thickness in gut tissue. The 16S rRNA gene analysis indicated that CTX exposure reshaped the gut microbiota diversity and community composition. Proteobacteria, Actinobacteriota and Bacteroidota were the most widely represented phyla in A. sinica gut. The exposure to CTX led to the absence of Verrucomicrobia in dominant phyla and an increase in Bacteroidota abundance. At the genus level, eleven genera with an abundance greater than 0.1% exhibited statistically significant differences among groups. Furthermore, changes in gut microbiota composition were accompanied by modifications in gut microbiota functions, with an up-regulation in amino acid and drug metabolism functions and a down-regulation in xenobiotic biodegradation and lipid metabolism-related functions under CTX exposure. Overall, our study enhances our understanding of the intestinal damage and microbiota disorder caused by the cefotaxime pollutant in aquatic invertebrates, which would provide guidance for healthy aquaculture.

NF-κB-coupled IL17 mediates inflammatory signaling and intestinal inflammation in Artemia sinica.

Nuclear factor-κB (NF-κB) plays a role as a rheostatic transcription factor in regulating intestinal inflammation, and its disruption or constitutive activation leads to inflammation and injury. However, the molecular mechanisms of NF-κB regulation remain largely unknown. In this study, the NF-κB-regulated host defenses against pathogen infections and facilitation of IL17 expression during stimulation with different bacteria were investigated. Intestinal inflammation was induced by dextran sulfate sodium, and NF-κB activity was inhibited in an intestinal injury model. Mannose receptor C type, ABF1/2, serpin B13, lysozyme, and ß-arrestin were significantly controlled by NF-κB in the inflamed intestinal tissue. High levels of NF-κB activation resulted in less pervasive intestinal damage and the maintenance of intestinal barrier integrity. Intestinal injury robustly increased the expression of IL17. NF-κB activation was enhanced by IL17 deficiency in the intestinal injury model. IL17 inhibition aggravated intestinal inflammation, leading to loss of epithelial architecture and the infiltration of inflammatory cells. These data suggest that NF-κB and IL17 play key mediator roles in the maintenance of gut epithelial integrity and immune homeostasis.