Time- and dose-dependent effects of bacterial infection on iron metabolism, inflammation, and oxidative stress in the juvenile soft-shelled turtle Pelodiscus sinensis.

Pathogen-induced high mortality is a severe problem in turtle cultures. Increasing evidence indicates that pathogenic infection may disrupt iron homeostasis, thereby creating a vicious cycle of iron imbalance-inflammation-oxidative stress. However, the effects of infection on iron metabolism and related physiological traits in turtles remain unclear. This study aimed to investigate the response of iron metabolism in juvenile soft-shelled turtles (Pelodiscus sinensis) under acute bacterial challenge and its association with inflammation and oxidative stress. We intraperitoneally injected juvenile P. sinensis (108 ± 2.5 g) with the recently identified pathogen Elizabethkingia anophelis at concentrations of 0, 3.24 × 107, 8.10 × 107, and 1.62 × 108 colony-forming units per millilitre (CFU/mL) in a volume of 0.2 mL. We sampled at 6, 24, and 120 h postinjection to assess the physiological responses to bacterial invasion. The results revealed that haemolysis developed as time progressed and the bacterial dose increased, accompanied by a decrease in plasma iron concentration. Moreover, the expression levels of iron metabolism-related genes in the liver and spleen-hepcidin, transferrin, TFR1, and FTH1-increased, whereas FPN1 expression decreased, concurrent with elevated tissue iron levels. Oxidative stress levels and the expression of proinflammatory cytokine genes were positively correlated with tissue iron accumulation. Overall, acute E. anophelis infection disrupts iron homeostasis in P. sinensis in a dose- and time-dependent manner, promotes the redistribution of iron from the circulation to storage tissues, exacerbates tissue inflammatory responses, and reduces antioxidant capacity. These findings indicate that dysregulated iron homeostasis plays a central role in infection-associated tissue injury and that restoring iron balance may aid in the treatment of bacterial infections in P. sinensis.