Intestinal inflammation, oxidative damage, and pathogenesis of intestinal <i>Cryptosporidium</i> in juvenile Asian sea bass (<i>Lates calcarifer</i>)

Abstract Piscine intestinal Cryptosporidium infection is a known cause of severe illness and mortality in juvenile Asian sea bass, with inflammation playing a central role. This inflammation triggers the generation of reactive oxygen species (ROS), leading to irreversible DNA damage and activation of apoptosis pathways. However, the specific impact of inflammation on ROS production, DNA damage, and apoptosis in this context remains unclear. This study investigated the pathogenic role of inflammation and ROS in causing DNA damage and cell apoptosis in piscine intestinal cryptosporidiosis. Forty‐four intestinal samples from 60‐ and 90‐day juvenile Asian sea bass were divided into four groups based on Cryptosporidium infection status. Histopathological evaluation and immunofluorescent analysis were conducted to assess ROS production, DNA damage, and cellular apoptosis markers. Results showed significantly higher inflammatory cell infiltration, intracellular ROS production, DNA damage, and cellular apoptosis in 60‐day infected fish compared to 90‐day infected fish. These findings underscore distinct responses in juvenile Asian sea bass to piscine intestinal cryptosporidiosis, highlighting severe inflammation, oxidative DNA damage, and cellular apoptosis, particularly in younger fish.