Abstract
Silver nanoparticles (AgNPs) are increasingly utilized in diverse fields due to their superior physical properties and antimicrobial effects. However, the continuous release of AgNPs into aquatic environments may pose potential hazards to aquatic animals and cause toxicological effects. Nevertheless, there is a lack of research regarding whether chronic exposure to AgNPs induces immunotoxicity that affects the susceptibility of aquatic animals to pathogens, and its precise mechanism of action remains largely unknown. Herein, by deploying AgNP stress and an aquatic reovirus (grass carp reovirus, GCRV) infection as a model system, we illustrated that exposure to AgNPs resulted in chronic oxidative stress and inflammatory effects in grass carp, which included the deposition of silver particles in tissues, impaired activity of antioxidant enzymes, overt tissue damage, imbalances of gut microbiota composition, and induction of inflammatory responses. Additionally, AgNPs exposure in conjunction with GCRV infection led to a noteworthy rise in viral loads and upregulation of pro-inflammatory genes, as compared to the control group. This work suggests that chronic stress by AgNPs may enhance susceptibility to aquatic virus infection through oxidative stress and inflammatory effects, providing fresh insights to elucidate the disease development in aquatic animals caused by heavy metal pollution.
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