Shell integrity is a key determinant of health in cultured bivalves; however, its damage may affect physiological and immune processes associated with repair. This study evaluated the effects of a single non-penetrating shell damage on cellular immune responses and immune-related gene expression in the mantle of the Pacific oyster Magallana gigas. Over 14 days post-damage, reactive oxygen species (ROS) and reactive nitrogen species (RNS) production, phagocytic activity, adhesion, and aggregation of hemocytes were assessed. Relative expression of tumor necrosis factor (TNF-1, TNF-2), interleukin-17 (IL-17-3, IL-17-6), and Toll receptor (Toll-1) genes was also determined in mantle tissue. The damage induced predominantly temporal alterations in hemocyte functional activity. During the first two days, ROS production decreased, while RNS production remained unchanged; phagocytic activity increased on day 1 and decreased on day 2. More prolonged changes were observed in hemocyte adhesion and aggregation. Of the genes examined, only TNF-2 showed a significant change, with decreased expression on day 7. These results show that a single non-penetrating shell damage primarily induces a broad stress-associated physiological response, which transiently modulates cellular immune parameters and local regulation mechanisms. By the end of the experiment, most parameters did not differ from the control, although certain changes persisted during shell repair.
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Lavrichenko et al. (2026) studied this question.
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