Effects of Elevated Temperature and Nickel Pollution On the Immune Status of Japanese Medaka

Changes in a host\u27s 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 degrees C (0.5 +/- degrees C) rapid increase in water temperature; or, both potential stressors in combination. Medaka maintained at room temperature (25 degrees C +/- 1 degrees 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 (O-2(center dot-)) 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 I 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 O-2(center dot-) 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 O-2(center dot-) production. Resting levels of extracellular O-2(center dot-) production was significantly reduced in fish maintained for I d at the elevated temperature. Effects on phorbol 12-myristate 13 acetate (PMA)-stimulated intracellular and extracellular O-2(center dot-) production were less dramatic than those observed for resting phagocytes. Exposure of medaka to elevated temperature for 14 d tended (p \u3c 0.06) to reduce PMA-stimulated intracellular O-2(center dot-) production (compared to the time-matched control). Although exposure of fish for 14 d to elevated temperature only slightly reduced stimulated extracellular O-2(center dot-) 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. (c) 2006 Elsevier Ltd. All rights reserved

Effects of inhaled ozone on pulmonary immune cells critical to antibacterial responses in situ

Effects of inhaled ozone on pulmonary immune cells critical to antibacterial responses in situ. Cohen MD, Sisco M, Baker K, Li Y, Lawrence D, van Loveren H, Zelikoff JT, Schlesinger RB. Department of Environmental Medicine, New York University School of Medicine, Tuxedo, New York 10987, USA. The goal of this study was to examine effects from repeated exposure to ozone (O3) on immune cells involved in cell-mediated antibacterial responses in the lungs. Rats exposed to 0.1 or 0.3 ppm O3 for 4 h/day, 5 days/wk, for 1 or 3 wk were analyzed for the ability to clear an intrapulmonary challenge with Listeria monocytogenes or had their lungs processed to obtain pulmonary alveolar macrophages (PAM) and lung-associated lymphocytes for analyses of select cell functions and surface marker expression. The results indicate that repeated inhalation exposure to O3 affected local cell-mediated immunity (CMI) responses as evidenced by effects on clearance of Listeria. However, this modulation was not consistently dependent on exposure concentration or duration. Short-term repeat exposures had more effect on host resistance than did the more prolonged regimen, with rats exposed to 0.1 ppm O3 most adversely impacted. Clearance patterns suggest modifications in innate resistance following 1 wk of exposure to 0.1 ppm O3, but no similar effect following a 3-wk regimen. Exposure to 0.3 ppm O3 appeared to affect both innate and acquired resistance after a 1-wk regimen, but mainly the former after an additional 2 wk of exposure. We conclude that these two mechanisms of resistance are differentially affected by O3 and that distinct time- and O3 concentration-dependent adaptation phenomena evolve for each; that is, in situ adaptation to higher levels of O3 may occur more readily with acquired than with innate/PAM-dependent resistance. A similar pattern of inconsistent effect on PAM and lung-associated lymphocytes was also evident. For example, while 3-wk exposures had a greater effect on PAM reactive oxygen intermediate ROI production, evidence for a significant effect on antibacterial activity was only notable among PAM from rats exposed for 1 wk. Among lung lymphocytes, while 3-wk exposure to 0.1 ppm O3 led to a significant increase in CD25 expression, there was no corresponding increase in responsivity to concanavalin A (ConA); only among cells from 1-wk-exposed rats did lymphoproliferative responses increase. Though investigations of altered immune cell cytokine receptor expression/binding activity are ongoing, results herein provide further evidence to support our longstanding hypothesis that some well-documented effects of O3 exposure on human health are quite likely linked to changes in local immune cell (i.e., PAM and lung-associated lymphocytes) functions, with the latter being related to changes in the capacities of these cells to interact with immunoregulatory cytokines