Molecular cloning of IL-6, IL-10, IL-11, IFN-ɤ and modulation of pro- and anti-inflammatory cytokines in cobia (Rachycentron canadum) after Photobacterium damselae subsp. piscicida infection

• Published in: Comparative Biochemistry and Physiology Part B: Biochemistry and Molecular Biology 2019-04, Vol.230, p.10-18
• Main Authors: Tran, Hung B., Chen, Shih-Chu, Chaung, Hso-Chi, Cheng, Ta-Chih
• Format: Article
• Language: English
• Subjects: Anti-inflammatory cytokines; Photobacterium damselae subsp. piscicida; Pro-inflammatory cytokines; Rachycentron canadum
• ISSN: 1096-4959; 1879-1107
• DOI: 10.1016/j.cbpb.2019.01.004

Photobacterium damselae subsp. piscicida (P. damselae subsp. piscicida) is the agent of Photobacteriosis, a serious fish disease that produces an acute infection and high mortality in farmed cobia. It has been proved that regulation of pro- and anti-inflammatory cytokines play a central role in initiation of proper inflammatory responses against bacterial infection. Here we have analyzed the expression of pro-inflammatory cytokines (IL-1β, TNF-α, IL-6, IL-8 and IFN-ɤ) and anti-inflammatory cytokines (IL-10 and IL-11) in spleen and head kidney during acute P. damselae subsp. piscicida infection of cobia. Our data revealed that cytokines tested showed distinct patterns of expression. While TNF-α and IL-8 showed a decay pattern of expression, IL-1β response was quite late. Moreover, P. damselae subsp. piscicida infection induced the simultaneous expressions of pro-inflammatory (IL-6, IFN-ɤ) and anti-inflammatory (IL-10, IL-11) cytokines. Together these results indicate the innate immunity of cobia is actively suppressed by P. damselae subsp. piscicida. •IL-6, IL-10, IL-11 and IFN-ɤ have been identified in cobia.•The expression pattern of cytokines was characterized by a depression of TNF-α and IL-8, a delayed response of IL-1β and simultaneous up-regulations of IL-6, IL-10, IL-11 and IFN-ɤ.•The cytokine disparity may explain the suppression of innate immunity by P. damselae subsp. piscicida in cobia.