Isolation and characterization of a human sperm antigen gene h-Sp-1.

BACKGROUND: Traumatic pancreatitis (TP) is a distinct subtype of pancreatitis. Although ferroptosis of pancreatic acinar cells is well documented in acute pancreatitis (AP), studies on ferroptosis in TP and its relationship with subsequent intra-abdominal infections (IAIs) remain limited and unclear. Incorporating predictive, preventive, and personalized medicine (3PM) strategies could significantly enhance TP management, particularly through early detection and targeted interventions.

METHODS: A total of 60 male rats were divided into four groups: TP model, ferroptosis activation, and inhibition groups. Physiological parameters, mortality rates, and serum cytokine, pancreatic enzyme expression, and oxidative stress factor levels were observed. Pathological evaluation of pancreatic tissue was performed. Subsequently, iron staining, ACSL4 immunofluorescence detection, and mRNA and protein expression of ferroptosis-related molecules were assessed in pancreatic tissues. Furthermore, 16S rDNA sequencing of peritoneal lavage fluid was performed to evaluate the impact of TP and ferroptosis modulation on the intra-abdominal microbiota and infection. Finally, clinical data from TP patients with IAIs were analyzed to identify commonalities with animal findings, offering predictive insights for human treatment.

RESULTS: TP caused severe pancreatic tissue damage, and activation of ferroptosis further exacerbated tissue damage, systemic inflammation, and animal mortality. Inhibition of ferroptosis improved these indicators in TP rats. Furthermore, 16S rDNA sequencing results showed that TP rats had enhanced intra-abdominal microbiota dysbiosis and an increased proportion of pathogenic bacteria. The use of ferroptosis activators further aggravated the IAIs in TP rats. Clinical analysis showed elevated serum ferroptosis biomarkers in TP patients, with higher proportions of antibiotic-resistant Acinetobacter and Pseudomonas aeruginosa found in abdominal cultures, highlighting the need for predictive biomarkers and personalized therapeutic strategies.

CONCLUSIONS: Inhibiting ferroptosis alleviates pancreatic damage and reduces mortality in TP rats. Ferroptosis exacerbates IAIs by increasing oxidative stress and inflammatory responses. From a 3PM perspective, targeting ferroptosis offers predictive and preventive potential, enabling earlier interventions and personalized therapies to improve patient outcomes and reduce complications.

SUPPLEMENTARY INFORMATION: The online version contains supplementary material available at 10.1007/s13167-025-00418-3.