PUBLICATION
Cortisol plays a role in the high environmental ammonia associated suppression of the immune response in zebrafish
- Authors
- Gonçalves, A.F., Neves, J.V., Coimbra, J., Rodrigues, P., Vijayan, M.M., Wilson, J.M.
- ID
- ZDB-PUB-170307-3
- Date
- 2017
- Source
- General and comparative endocrinology 249: 32-39 (Journal)
- Registered Authors
- Keywords
- Acute phase response, Ammonia, Cortisol, Innate immunity, Mifepristone, Zebrafish
- MeSH Terms
-
- Acute-Phase Proteins/metabolism
- Altitude*
- Ammonia/adverse effects*
- Animals
- Environment*
- Gene Expression Regulation/drug effects
- Hydrocortisone/metabolism*
- Immunity*/drug effects
- Immunity*/genetics
- Lipopolysaccharides/pharmacology
- RNA, Messenger/genetics
- RNA, Messenger/metabolism
- Zebrafish/genetics
- Zebrafish/immunology*
- Zebrafish Proteins/genetics
- Zebrafish Proteins/metabolism
- PubMed
- 28263819 Full text @ Gen. Comp. Endocrinol.
Citation
Gonçalves, A.F., Neves, J.V., Coimbra, J., Rodrigues, P., Vijayan, M.M., Wilson, J.M. (2017) Cortisol plays a role in the high environmental ammonia associated suppression of the immune response in zebrafish. General and comparative endocrinology. 249:32-39.
Abstract
Exposure to high environmental ammonia (HEA) levels increases the vulnerability of fishes to parasitic, viral and bacterial diseases. We tested the hypothesis that elevated plasma cortisol levels plays a role in the HEA-mediated immunosuppression in fishes. To this end, we tested the effect of exogenous cortisol treatment on lipopolysaccharide (LPS)-induced immune response in zebrafish (Danio rerio). Also, to test whether GR signaling is involved in HEA-mediated immunosuppression, zebrafish were treated with mifepristone, a glucocorticoid receptor antagonist, and the LPS-induced immune response assessed after HEA exposure. We evaluated a panel of important immunity-related genes including interleukin 1β (il1b) and suppressor of cytokine signaling (socs-1a, 2, 3) and acute phase response genes [serum amyloid A (saa), transferrin (tfa), leukocyte cell-derived chemotaxin 2-like (lect2l), haptoglobin (hp), hepcidin (= hepatic anti-microbial peptide hamp), and complement component 3b (c3b)] by real-time quantitative PCR. Our results demonstrate that exogenous cortisol administration as well as elevated cortisol levels in response to HEA exposure modulate mRNA transcript levels of key mediators of the innate immune response in zebrafish. Mifepristone treatment reduced whole body cortisol levels and eliminated the HEA-mediated changes in transcript abundance of socs1a, il1b, as well as APR genes. Together, these results suggest that the HEA effect on innate immune response is in part mediated by cortisol signaling, while the mode of action, inlcuding the receptors involved remains to be elucidated.
Genes / Markers
Expression
Phenotype
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Fish
Orthology
Engineered Foreign Genes
Mapping