Staphylococcus aureus has been recognized as an important foodborne pathogen. However, knowledge about the epidemiology and genetic characteristics of S. aureus in the meat production chain from farm to market is limited. The aim of this study was to investigate the genetic characteristics of S. aureus in animal samples isolated from Xinjiang province farms and farmer’ markets, by determining staphylococcal protein A (spa) repeat region and virulence factor typing, and by assessment of antimicrobial resistance. Out of 1324 samples, 128 (9.7%) were positive for S. aureus, 26 (2.0%) of them were identified as methicillin-resistant S. aureus (MRSA) and 88 (6.6%) of them were identified as vancomycin-resistant S. aureus (VRSA). Antimicrobial resistance was determined using the disk diffusion method. S. aureus isolates showed resistance to penicillin G (98.4%), clarithromycin (69.5%), erythromycin (69.5%), vancomycin (68.8%), and tetracycline (67.2%). A total of 80.4% of isolates showed resistance to three or more antimicrobial classes. PCR was used to detect ten virulence genes such as the enterotoxin (sea, seb, and sec), hemolysin (hla and hlb), clumping factor (clfA), and fibronectin-binding proteins A and B (fnbA and fnbB). Our study showed that isolates harbored two or seven virulence genes. All strains encode hla and clfA, and half of them encode hlb and enterotoxin genes. The spa typing results showed that the 128 isolates were grouped into 32 spa types. The main spa types were t127 (22.7%), t2592 (12.5%), t437 (10.9%), and t2616 (10.9%). Notably, isolates of t437 type accounted for 46.2% of the MRSA. Our data indicate that meats in the slaughterhouse and farmers' markets were contaminated with S. aureus. S. aureus virulence genes and spa types were diverse, and its antibiotic resistance was serious. The presence of MRSA and VRSA represents potential public health risks and warrants further investigation regarding the driving factors of such resistance and their transmission to humans.

Both the jejunum and colon release cytokines that interact with intestinal microbiota. However, it is largely unclear which cytokines and microbial populations are involved in the homeostasis of the intestinal ecosystem for sheep health. To address this, we collected contents for isolating microbiota and tissues for determining cytokines from the jejunum and colon of 7-month-old Altay sheep. We used the techniques of 16S rRNA sequencing and ELISA to detect microbial population and cytokine level, respectively. Correlations between microbial population and cytokines were analyzed by Spearman correlation coefficient. The correlation analysis revealed higher populations of Bacteroides, Fibrobacteres and Spirochetes in the colon than in the jejunum, and IL-6 and IL-12 levels were higher in the jejunum than in the colon. Association analysis further revealed a positive association between IL-10 level and both Ruminococcus_2 and norank_f_Bifidobacteriaceae population in the jejunum. The analysis also revealed positive associations between IL-6 level and Ruminococcaceae_UCG-014 and Ruminococcaceae_UCG-013 population, IL-10 and Prevotellaceae_UCG-004, as well as TNF-α and Prevotellaceae_UCG-003 in the colon. These results indicate a potential interaction between the intestinal microbiota and the host immune system that needs to be further clarified for considering dietary formulations to maintain animal health and disease prevention.

Background: Shiga toxin-producing Escherichia coli ( STEC ) is a leading foodborne pathogen responsible for hemolytic uremic syndrome (HUS). This pathogen poses a severe threat to global public health. MicroRNAs (miRNAs) are increasingly recognized as essential post-transcriptional regulators and therapeutic targets. Despite this, their exact regulatory networks and roles in STEC pathogenesis remain largely unknown. Methods: An in vitro infection model was established using human intestinal epithelial cells (HIECs), with optimal infection time and bacterial load determined via CCK-8 assays and DAPI staining. High-throughput RNA sequencing (RNA-seq) was performed to profile miRNA and mRNA expression, followed by RT-qPCR validation. Differentially expressed miRNAs and their target mRNAs were identified by integrating miRanda predictions with transcriptomic data. Target functions were annotated using GO and KEGG enrichment analyses. A protein–protein interaction (PPI) network was constructed to identify core hub genes, and upstream transcription factors (TFs) were predicted using the TRRUST and hTFtarget databases, culminating in the construction of an integrated miRNA–hub mRNA–TF regulatory network. Results: Infection of HIECs with STEC (10 ⁶ CFU/mL) for 1 hour induced profound cellular structural damage, accompanied by the differential expression of 652 target mRNAs (301 upregulated and 351 downregulated). Functional enrichment revealed that these targets are predominantly involved in inflammatory responses, apoptosis, and cell proliferation. Through the PPI network, 10 core hub genes (including TNF, CXCL8, CCN2, and TGFB2) were identified, along with 11 highly correlated regulatory TFs. Based on the integrated network analysis, has-miR-3121-3p, hsa-miR-219b-5p, and hsa-miR-543 were pinpointed as master regulatory miRNAs, suggesting they orchestrate critical host signaling pathways during infection. Conclusion: STEC infection drastically reprograms the transcriptomic landscape of HIECs, triggering the dysregulation of inflammation and apoptosis-related pathways. This study is the first to delineate a comprehensive miRNA–mRNA–TF regulatory network for STEC infection, highlighting miR-3121-3p, miR-219b-5p, and miR-543 as key molecular mediators. These findings provide novel insights into the molecular pathogenesis of STEC and lay a crucial foundation for exploring potential regulatory and host-directed therapeutic targets.