Effects of elevated temperature and nickel pollution on the immune status of Japanese medaka

Changes in a hostʹs environment (i.e. physical or chemical) can alter normal immune function. In aquatic organisms, exposure to stress can result in significant changes in innate immunity. In the natural environment, fish are exposed to multiple stressors simultaneously. Temperature change and/or chemical exposure as individual environmental stressors have been shown in various fish species to alter all aspects of the immune response. These same stressors have also been shown to alter plasma steroid levels in exposed fish. For this study, the effects of elevated temperature and nickel pollution on specific immune parameters of Japanese medaka (Oryzias latipes) were determined. Fish were exposed for 1, 7 or 14 d to either: waterborne nickel (Ni) at the nominal concentration of 125 ppb; a 5 °C (±0.5 °C) rapid increase in water temperature; or, both potential stressors in combination. Medaka maintained at room temperature (25 °C ± 1 °C) served as the controls. Altered function of the innate and adaptive arms of the immune response was evaluated by assessing kidney macrophage-mediated superoxide (O2−) production and splenic T-cell proliferation, respectively. Plasma cortisol levels were analysed in the same fish as a marker of the physiological stress response. While kidney cell number was unaffected by exposure of fish to either stressor alone or both factors in combination, spleen cellularity was decreased (compared to control fish) in medaka exposed for 1 d to thermal stress in combination with Ni, and to a lesser extent to thermal stress alone. T-lymphocyte proliferation by medaka splenocytes was not affected by any exposure paradigm. Unstimulated intracellular O2− production by kidney phagocytes was significantly elevated (compared to control) in medaka exposed for 1 d to either thermal stress alone or temperature change in combination with Ni; by 7 d, only the stressor combination significantly increased baseline O2− production. Resting levels of extracellular O2− production was significantly reduced in fish maintained for 1 d at the elevated temperature. Effects on phorbol 12-myristate 13 acetate (PMA)-stimulated intracellular and extracellular O2− production were less dramatic than those observed for resting phagocytes. Exposure of medaka to elevated temperature for 14 d tended (p < 0.06) to reduce PMA-stimulated intracellular O2− production (compared to the time-matched control). Although exposure of fish for 14 d to elevated temperature only slightly reduced stimulated extracellular O2− production, exposure for the same duration to Ni alone significantly depressed oxyradical production by kidney phagocytes (compared to the time-matched controls). Decreased plasma cortisol levels were observed in fish exposed for 7 d to either an elevated water temperature or Ni (compared to the time-matched control); by 14 d of exposure, no significant treatment-induced effects on cortisol levels were observed. These findings add to the growing body of literature seeking to determine what effects, if any, exposure to multiple aquatic pollution-induced effects have upon fish health and the health of impacted ecosystems.