TY - JOUR
T1 - Transgenic expression of tilapia piscidin 3 (TP3) in zebrafish confers resistance to Streptococcus agalactiae
AU - Su, Bor Chyuan
AU - Lai, Yung Wei
AU - Chen, Jyh Yih
AU - Pan, Chieh Yu
N1 - Funding Information:
This study was partially supported by funding ( 105-2321-B-001-032 -, 103-2313-B-001-007-MY3 , 105-2811-B-001-056 -) from the Ministry of Science and Technology, R.O.C . to Mr. Jyh-Yih Chen. Research funding was also received from the Marine Research Station (Jiaushi, Ilan), Institute of Cellular and Organismic Biology, Academia Sinica, Taiwan , to Mr. Jyh-Yih Chen. We thank Dr. Marcus Calkins at the editorial office of the Institute of Cellular and Organismic Biology for language editing.
Funding Information:
This study was partially supported by funding (105-2321-B-001-032-, 103-2313-B-001-007-MY3, 105-2811-B-001-056-) from the Ministry of Science and Technology, R.O.C. to Mr. Jyh-Yih Chen. Research funding was also received from the Marine Research Station (Jiaushi, Ilan), Institute of Cellular and Organismic Biology, Academia Sinica, Taiwan, to Mr. Jyh-Yih Chen. We thank Dr. Marcus Calkins at the editorial office of the Institute of Cellular and Organismic Biology for language editing.
PY - 2018/3/1
Y1 - 2018/3/1
N2 - 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.
AB - 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.
KW - Streptococcus agalactiae
KW - Tilapia piscidin 3
KW - Zebrafish
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U2 - 10.1016/j.fsi.2018.01.001
DO - 10.1016/j.fsi.2018.01.001
M3 - Article
C2 - 29317307
AN - SCOPUS:85043388671
SN - 1050-4648
VL - 74
SP - 235
EP - 241
JO - Fish and Shellfish Immunology
JF - Fish and Shellfish Immunology
ER -