Xanthine oxidase activity exerts a pro-oxidant and pro-inflammatory profile in gills of experimentally infected silver catfish with Streptococcus agalactiae

Abstract

Some studies have demonstrated that xanthine oxidase activity, through the regulation of uric acid levels, exerts a pro-inflammatory profile during infectious diseases. It has been recognized that uric acid induces the release of pro-inflammatory mediators, such as reactive oxygen species (ROS) and nitric oxide (NO), which contribute to inflammatory processes. Considering this, the aim of this study was to evaluate whether upregulation of branchial xanthine oxidase activity may be considered a pathway involved in ROS and nitric oxide (NOx) metabolites production in experimentally infected Rhamdia quelen (silver catfish) with Streptococcus agalactiae. Xanthine oxidase activity, and uric acid, ROS and NOx levels increased in gills of infected animals compared to uninfected animals. Moreover, a positive Pearson correlation was observed between uric acid and ROS levels, and between uric acid and NOx levels. Histopathology revealed the presence of necrosis, hyperplasia and vein congestion in gills of animals infected with S. agalactiae. Based on this evidence, the upregulation of xanthine oxidase activity induces a pro-inflammatory and oxidative profile in the gills of fish infected with S. agalactiae. The excessive uric acid levels induce the release of pro-inflammatory mediators, such as ROS and NOx, which contribute to disease pathogenesis. In summary, the upregulation of xanthine oxidase activity may be considered a pathway involved in ROS and NOx production.