BCL10 regulates the production of proinflammatory cytokines by activating MAPK–NF–κB/Rel signaling pathway in oysters.

B cell lymphoma/leukemia 10 (BCL10) is an important member of the caspase recruitment domain-containing (CARD) protein family, which plays crucial roles in mediating the host inflammatory response. In the present study, a BCL10 homologue was identified from Pacific oyster Crassostrea gigas (designed as Cg BCL10). The full length cDNA of Cg BCL10 was of 897 bp with an open reading frame of 522 bp encoding a polypeptide of 174 amino acids containing a classical CARD domain. The deduced amino acid sequence of Cg BCL10 shared low similarity with the previously identified BCL10s from other species. In the phylogenetic tree, Cg BCL10 was firstly clustered with Cv BCL10 from Crassostrea virginica and then assigned into the branch of invertebrate BCL10s. The mRNA transcripts of Cg BCL10 were highly expressed in gonad, gill, adductor muscle, and haemocytes. After Vibrio splendidus stimulation, the mRNA expression level of Cg BCL10 in haemocytes increased significantly (p < 0.01) at 24, 72 and 96 h. In Cg BCL10-RNAi oysters, the phosphorylation level of mitogen-activated protein kinases (MAPKs), nuclear translocation of NF-κB/Rel and activator protein-1 (AP-1) in haemocytes were inhibited, and the mRNA expressions of inflammatory cytokines including Cg IL17-1, Cg IL17-2, Cg IL17-3, Cg IL17-6 and Cg TNF all decreased significantly (p < 0.01) at 12 h after V. splendidus stimulation. These results suggested that Cg BCL10 regulated the expression of inflammatory cytokines by activating MAPK kinase, and nuclear translocation of NF-κB/Rel and AP-1 to defense pathogen. • A BCL10 homologue (Cg BCL10) was identified from oyster. • The expression of Cg BCL10 in haemocytes was up-regulated after the stimulation of V. splendidus. • Cg BCL10 mediated the phosphorylation of Cg JNK and Cg P38 to activate MAPK inflammatory signaling pathway. • BCL10 regulated Cg NF-κB/Rel and Cg AP-1 to promote the production of inflammatory cytokines. [ABSTRACT FROM AUTHOR]