ZFIN ID: ZDB-PUB-180111-5
Transgenic expression of tilapia piscidin 3 (TP3) in zebrafish confers resistance to Streptococcus agalactiae
Su, B.C., Lai, Y.W., Chen, J.Y., Pan, C.Y.
Date: 2018
Source: Fish & shellfish immunology   74: 235-241 (Journal)
Registered Authors: Pan, Chieh-Yu
Keywords: Streptococcus agalactiae, Tilapia piscidin 3, Zebrafish
MeSH Terms:
  • Animals
  • Animals, Genetically Modified/genetics
  • Animals, Genetically Modified/immunology
  • Animals, Genetically Modified/metabolism
  • Cichlids*/genetics
  • Cichlids*/immunology
  • Disease Resistance/genetics*
  • Disease Resistance/immunology
  • Fish Diseases/genetics*
  • Fish Diseases/immunology*
  • Fish Proteins*/genetics
  • Fish Proteins*/metabolism
  • Streptococcal Infections/genetics
  • Streptococcal Infections/immunology
  • Streptococcal Infections/veterinary*
  • Streptococcus agalactiae/physiology
  • Zebrafish/genetics*
  • Zebrafish/immunology
  • Zebrafish/metabolism
PubMed: 29317307 Full text @ Fish Shellfish Immunol.
To study the biological role of tilapia piscidin 3 (TP3) in Streptococcus agalactiae infection in vivo, TP3/DsRed overexpressing transgenic zebrafish were generated. Under normal growth conditions, TP3/DsRed transgenic zebrafish exhibited an orange-red body color, without any other obvious abnormalities. However, when compared to wild type fish, TP3/DsRed transgenic zebrafish were resistant to S. agalactiae infection. After infection, the TP3 overexpressing fish exhibited higher expression of Toll-like receptor 4a (TLR4a), interleukin (IL)-10, IL-22, and C3b. Furthermore, TP3/DsRed transgenic zebrafish exhibited reduced induction of proinflammatory cytokines, including TNFα, IL-1β, IL-21, MyD88, and nuclear factor (NF)-κB. Taken together, our data show that TP3 overexpression in zebrafish can effectively suppress proinflammatory responses and enhance production of C3b. Together, these actions are conducive to the resolution of inflammation and bacterial clearance. We further postulate that TP3 may exert its anti-inflammatory effects by enhancing TLR4a-mediated negative regulation of NF-κB.