Acute hypoxia-reperfusion triggers immunocompromise in Nile tilapia

被引:52
作者
Choi, K.
Lehmann, D. W.
Harms, C. A.
Law, J. M. [1 ]
机构
[1] N Carolina State Univ, Coll Vet Med, Dept Populat Hlth & Pathobiol, Raleigh, NC 27695 USA
[2] N Carolina State Univ, Dept Environm & Mol Toxicol, Raleigh, NC 27695 USA
[3] N Carolina State Univ, Coll Vet Med, Dept Clin Sci, Raleigh, NC 27606 USA
关键词
D O I
10.1577/H06-010.1
中图分类号
S9 [水产、渔业];
学科分类号
0908 ;
摘要
Inadequate dissolved oxygen in the aquatic environment is a well-established cause of fish morbidity and mortality. The specific effects of hypoxia on immune function in fish, however, are not well characterized. In this study, the effects of acute hypoxia followed by reoxygenation (rapid tissue reperfusion) as a source of immunocompromise in Nile tilapia Oreochromis niloticus were investigated. Using a precision apparatus developed in our laboratory for hypoxia exposures, a series of assays of increasing specificity for immune function were performed on acutely hypoxia-stressed Nile tilapia: tier I consisted of histopathology, tier 11 of hematology, plasma chemistry, and determining cortisol concentration, and tier III of determining the phagocytic index and analyzing the expression of the cytokines transforming growth factor-beta (TGF-beta) and interleukin-1 beta (IL-1 beta). Nile tilapia were exposed to 7% oxygen saturation for 96 h, then tank water was rapidly reoxygenated. Sampling intervals were 48 and 96 h during hypoxia and 12 and 84 It during reperfusion. Histopathology showed no remarkable microscopic abnormalities in lymphoid or other tissues. Lymphopenia and neutrophilia were observed in peripheral blood. Plasma total protein, partial pressure of oxygen, and oxygen saturation were decreased in response to hypoxia. Plasma lipase decreased in response to hypoxia but returned to normal during reperfusion. Phagocytic capability and the phagocytic index decreased during hypoxia and 12 It reperfusion, whereas these values were recovered by 84 It reperfusion. The TGF-beta transcription continued to increase during the exposures, the greatest production being at 12 It reperfusion, whereas IL-I beta transcription decreased in response to hypoxia and reperfusion. We conclude that acute hypoxia triggered an overall downregulation of the immune system in the test fish. This suggests a possible factor in the pathogenesis of disease outbreaks in fish in which repeated, sublethal bouts of environmentally induced hypoxia lead to increased disease susceptibility and individual mortalities rather than massive fish kills.
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收藏
页码:128 / 140
页数:13
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