Evaluation of Ammonia Nitrogen Exposure in Immune Defenses Present on Spleen and Head-Kidney of Wuchang Bream ( Megalobrama amblycephala )

• Published in: International journal of molecular sciences 2022-03, Vol.23 (6), p.3129
• Main Authors: Guo, Honghui, Chen, Siqi, Ouyang, Kang, Kuang, Yu, Yang, Hui, Wang, Yingying, Tang, Rong, Zhang, Xi, Li, Dapeng, Li, Li
• Format: Article
• Language: English
• Subjects: Adaptive immunity; Ammonia; Animals; Aquaculture; Aquatic ecosystems; Bream; Cortisol; Cyprinidae - genetics; Cypriniformes; Ecosystem; Exposure; Fish; Fish Diseases; Fish Proteins - genetics; Gene expression; head-kidney; IL-1β; Immune response; Immune system; immunity; Immunity, Innate; Immunoglobulin M; Innate immunity; Kidney - metabolism; Kidneys; Lysozyme; Megalobrama amblycephala; Molecular modelling; mRNA; MyD88 protein; Myeloid Differentiation Factor 88 - metabolism; Nitrogen; Proteins; Spleen; Spleen - metabolism; stress; Toll-like receptors; Tumor necrosis factor-α
• ISSN: 1422-0067; 1661-6596; 1422-0067
• DOI: 10.3390/ijms23063129

Ammonia is one of the most important environmental factors in aquatic ecosystems. However, there are limited studies on the effects of chronic or long-term ammonia stress and its potential molecular mechanism in fish. This study aimed to investigate the immune response and molecular mechanisms in the spleen and head-kidney of fish following chronic ammonia exposure. (9.98 ± 0.48 g) were exposed to different concentrations of total ammonia nitrogen (0-30 mg/L) for 30 days. Ammonia exposure caused significant increases in cortisol levels and decreases in lysozyme and complement 3/4 concentrations in the serum, indicating inhibitory effects of ammonia stress on innate immune responses. Ammonia exposure also induced concentration-dependent increases in ammonia concentrations in tissue, pathological damage and indexes of spleen and head-kidney. Additionally, the contents of immunoglobulin M (IgM), interleukin 1β (IL-1β) and tumor necrosis factor α (TNF-α) as well as mRNA levels of toll-like receptors (TLRs)/Myeloid differentiation factor 88 (MyD88)-independent signaling molecules in the spleen and head-kidney were significantly downregulated after ammonia exposure. Our findings suggested that chronic ammonia exposure caused the suppression of innate and adaptive immune responses through downregulating TLR/MyD88-independent signaling. Adverse influences of chronic ammonia stress were more severe in the spleen than in the head-kidney.