Abstract:In mammals, Toll-IL-1 receptor (TIR) domain-containing adaptor molecule 1 (TICAM-1) is a signaling adaptor for TLR3 and TLR4 that activates the transcription factors IRF-3, NF-κB, and AP-1, leading to the induction of type I interferon and cytokines. TICAM is also identified in some fish species, however, the gene expression profiling of TICAM is largely unknown in teleosts. Because bacteria such as Aeromonas hydrophila, Streptococcus spp. and Edwardsiella tarda and viruses such as channel catfish virus cause a multisystemic disease responsible for severe losses in channel catfish aquaculture in China. In this study, gene expression profiling of TICAM in different immune tissues(liver, headkidney, spleen，and intestine) after infection with these pathogens assayed by quantitative RT-PCR was described. After infection with A. hydrophila, TICAM was up-regulated approximately 2.3-fold at 24 h in liver and 1.9-fold at 12 h in spleen, while expression of this gene was down-regulated in headkidney and intestine, with the lowest expression as 0.15-fold at 48 h in headkidney, 0.53-fold at 24 h in intestine, respectively. TICAM was up-regulated drastically in liver, spleen, headkidney and intestine after infection with Streptococcus spp. It reached the highest level with 23-fold in liver at 7 d post infection, and it increased about 10 times in headkidney and spleen after infection. The expression of TICAM increased in all tested tissues after infection with E.tarda, especially it was up regulated to the highest （23.1-fold) at 7d in spleen. After infection with channel catfish virus, the gene TICAM expression was up-regulated in liver, headkidney and intestine moderately, with the highest expression of 3.7-fold in liver at 72 h, 2.8-fold in headkidney at 7 d, 1.5-fold at 24 h in intestine. However, it was down-regulated in spleen,and its lowest expression was 0.13-fold at 24 h. In conclusion, the results of this study suggest that the TICAM gene may play crucial roles in innate immunity in channel catfish.
