Vasoactive intestinal peptide (VIP), a member of secretin/glucagon family, is involved in a variety of biological activities such as gut motility, immune responses, and carcinogenesis. In this study, the VIP precursor gene (On-VIP) and its receptor gene VIPR1 (On-VIPR1) were identified from Nile tilapia (Oreochromis niloticus), and the functions of On-VIP in the immunomodulation of Nile tilapia against bacterial infection were investigated and characterized. On-VIP and On-VIPR1 contain a 450 bp and a 1326 bp open reading frame encoding deduced protein of 149 and 441 amino acids, respectively. Simultaneously, the transcript of both On-VIP and On-VIPR1 were highly expressed in the intestine and sharply induced by Streptococcus agalatiae. Moreover, the positive signals of On-VIP and On-VIPR1 were detected in the longitudinal muscle layer and mucosal epithelium of intestine, respectively. Furthermore, both in vitro and in vivo experiments indicated several immune functions of On-VIP, including reduction of P65, P38, MyD88, STAT3, and AP1, upregulation of CREB and CBP, and suppression of inflammation. Additionally, in vivo experiments proved that On-VIP could protect Nile tilapia from bacterial infection and promote apoptosis and pyroptosis. These data lay a theoretical basis for further understanding of the mechanism of VIP guarding bony fish against bacterial infection.

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Heme oxygenase-1 (HO-1) is a stress-inducible enzyme with antioxidant, anti-inflammatory, and anti-apoptotic effects. In this study, the HO-1 gene from Litopenaeus vannamei (Lv-HO-1) was identified. The open reading frame of Lv-HO-1 is 747 bp, encoding a peptide of 248 amino acids as well as a conserved HemO structural domain. Lv-HO-1 is 70–90% homological to crustaceans and about 50% homological to arthropods. The transcript levels of Lv-HO-1 were highest in the hepatopancreas and lower in other tissues. Knockdown of Lv-HO-1 led to structural destruction of the hepatopancreas. After ammonia exposure, Lv-HO-1 was significantly induced. Knockdown of Lv-HO-1 during ammonia exposure resulted in a significant decrease in antioxidant capacity and cellular autophagy levels compared to the control and increased apoptosis. The transcriptional levels of SOD and GSH-Px were considerably reduced (p < 0.05), as were the transcriptional levels of Atg3, Atg4, Atg5, and Atg10. The results indicated that Lv-HO-1 from L. vannamei can be induced by oxidative stress and may have important roles in regulating the host antioxidant system, reducing cell apoptosis.