Title of article :
Molecular cloning and expression analysis of two lipopolysaccharide-induced TNF-α factors (LITAFs) from rock bream, Oplegnathus fasciatus
Author/Authors :
Hwang، نويسنده , , Seong Don and Shim، نويسنده , , Sang Hee and Kwon، نويسنده , , Mun-Gyeong and Chae، نويسنده , , Young Sun and Shim، نويسنده , , Won Joon and Jung، نويسنده , , Jee-Hyun and Kim، نويسنده , , Ju-Won and Park، نويسنده , , Chan-Il، نويسنده ,
Issue Information :
روزنامه با شماره پیاپی سال 2014
Pages :
8
From page :
467
To page :
474
Abstract :
Lipopolysaccharide (LPS)-induced tumor necrosis factor (TNF)-α factor (LITAF) plays an important role controlling the expression of TNF-α and the other cytokine genes in the presence of LPS. However, two LITAF homologues have not been characterized in fish. In this study, we cloned two distinct LITAF (RbLITAF1 and RbLITAF2) cDNAs from rock bream (Oplegnathus fasciatus) and characterized their expression profiles after infection with Edwardsiella tarda, Streptococcus iniae or red seabream iridovirus (RSIV). The coding regions of RbLITAF1 and RbLITAF2 cDNAs were 492 bp and 417 bp, encoding 153 and 138 amino acid residues, respectively. The genes consisted of a LITAF domain. RbLITAF1 was highly expressed in the spleen and heart of healthy rock bream, whereas RbLITAF2 was highly expressed in the gill, intestine and stomach. In spleen, the gene expression of RbLITAF1 and RbLITAF2 were increased until 5 days post-infection (dpi), and then decreased at 7 dpi. In kidney, E. tarda and RSIV infection led to induction of the RbLITAF1 gene at 1 dpi, RbLITAF2 gene was down-regulated after pathogen infection. These results suggest that RbLITAFs may be involved in the LITAF-mediated immune response and regulate systemic immune responses against pathogen infection.
Keywords :
LITAF , Edwardsiella tarda , Red seabream iridovirus , Streptococcus iniae , Oplegnathus fasciatus
Journal title :
Fish and Shellfish Immunology
Serial Year :
2014
Journal title :
Fish and Shellfish Immunology
Record number :
2112936
Link To Document :
بازگشت