Abstract

A 100-day feeding trial was conducted to investigate the influences of dietary lipid levels on the immunity and mechanism in abalone Haliotis discus hannai Ino. Abalones (initial weight: 10.98 ± 0.05 g) were fed with graded levels of dietary lipid, which were 15.73, 23.41, 31.72, 38.25, 46.35, 55.63, 61.70 and 67.19 g/kg. Results showed that compared with the treatment with 38.25 g/kg of dietary lipid, 67.19 g/kg of dietary lipid increased the cumulative mortality of abalone after a challenge with Vibrio parahaemolyticus. Meanwhile, 67.19 g/kg of dietary lipid decreased the activities of lysozyme (LZ) and acid phosphatase (ACP) in serum, and the mRNA levels of β-defensin and mytimacin 6 in hepatopancreas of abalone. The mRNA levels of tumour necrosis factor α (tnfα), activator protein 1 (ap-1), nuclear factor κB (nf-κb), interleukin 1 receptor-associated kinase-4 (irak4), myeloid differentiation primary response protein MyD88 (myd88), toll-like receptor 2 (tlr2), tlr4 and perilipin-2, and the protein level of interleukin-1β (IL-1β), TNFα, NF-κBp65, AP-1, MyD88 and Perilipin-2 in hepatopancreas were up-regulated by 67.19 g/kg of dietary lipid. However, the mRNA levels of arginase and inhibitor of κBα (iκbα) were down-regulated. Besides, 67.19 g/kg of dietary lipid up-regulated the mRNA levels of executor apoptosis-related cysteine peptidase 3 (caspase-3), caspase-7 and B-cell lymphoma protein-2-associated X protein (bax), and the protein levels of caspase-3 and c-Jun N-terminal kinases (JNK) in hepatopancreas. Moreover, high dietary lipid level down-regulated the mRNA levels of copper/zinc superoxide dismutase (cuznsod), manganese superoxide dismutase (mnsod), catalase (cat), glutathione peroxidase (gpx), glutathione-S-transferase (gst) and NF-E2-related factor 2 (nrf2), while up-regulated the mRNA and protein levels of Kelch-like ECH-associated protein 1 (Keap1) in hepatopancreas. It was concluded that a high level (67.19 g/kg) of dietary lipid decreased the immunity of abalone, which might be related to the aggravated inflammation and apoptosis, and decreased anti-oxidative capacity under Perilipin-2/TLRs/MyD88/IRAK4/(NF-κB or AP-1), JNK/Bcl-2/Bax and Keap1/Nrf2 signalling.

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