Document Detail

Acute hypoxia-reperfusion triggers immunocompromise in Nile tilapia.
MedLine Citation:
PMID:  18201054     Owner:  NLM     Status:  MEDLINE    
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 II 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-1beta (IL-1beta). 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 h 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 h reperfusion, whereas these values were recovered by 84 h reperfusion. The TGF-beta transcription continued to increase during the exposures, the greatest production being at 12 h reperfusion, whereas IL-1beta 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.
K Choi; D W Lehmann; C A Harms; J M Law
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  Journal of aquatic animal health     Volume:  19     ISSN:  0899-7659     ISO Abbreviation:  J. Aquat. Anim. Health     Publication Date:  2007 Jun 
Date Detail:
Created Date:  2008-01-18     Completed Date:  2008-02-19     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  9884881     Medline TA:  J Aquat Anim Health     Country:  United States    
Other Details:
Languages:  eng     Pagination:  128-40     Citation Subset:  IM    
Department of Environmental and Molecular Toxicology, North Carolina State University, Raleigh, North Carolina 27695, USA.
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MeSH Terms
Anoxia / blood,  immunology,  veterinary*
Blood Chemical Analysis / veterinary
Blood Gas Analysis
Cichlids / blood*,  immunology*
Cytokines / biosynthesis
Hematologic Tests / veterinary
Hydrocortisone / blood
Interleukin-1beta / biosynthesis
Oxygen / pharmacology*
Phagocytosis / drug effects
Reperfusion / veterinary*
Time Factors
Transforming Growth Factor beta / biosynthesis
Reg. No./Substance:
0/Cytokines; 0/Interleukin-1beta; 0/Transforming Growth Factor beta; 50-23-7/Hydrocortisone; 7782-44-7/Oxygen

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine

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