Abstract
Increasing evidence indicates that viral infections can disrupt iron metabolism, thereby contributing to the onset and progression of viral infection-related diseases. Ferritin exerts immunosuppressive and proinflammatory functions during viral infection. Previous integrated transcriptomics and proteomics analyses, aimed at elucidating the resistance mechanisms of Larimichthys crocea against large yellow croaker iridovirus (LYCIV), have suggested that ferritin middle-subunit may confer a potential advantage. To elucidate the immunity-protecting roles of ferritin middle-subunit from large yellow croaker (LcferM) against LYCIV infection, the molecular characterization and immune function of LcferM were analyzed. The open reading frame of LcferM is 531 bp, encoding 176 amino acids. LcFerM shows the highest identity with the ferritin middle-subunit of sea bream (Sparus aurata). Recombinant LcFerM protein (r-LcFerM) significantly enhanced the respiratory burst capacity of large yellow croaker head kidney macrophages (LCM) cells and effectively alleviated apoptosis induced by the double-stranded DNA virus analog poly (dA: dT). Transcriptomic analysis following LcferM overexpression influences multiple key biological processes and signaling pathways, including cytosolic ribosome, cytosolic small ribosomal subunit, C-type lectin receptor, and MAPK signaling pathways. The regulation of these pathways indicates that LcferM comprehensively enhances macrophage immune function through multiple mechanisms, promoting pathogen clearance and maintaining immune system homeostasis. The results from the present study provide sequence, expression, and anti-LYCIV functional information of LcferM, laying the foundation for achieving resistance to LYCIV in large yellow croaker breeding.