Genes encoding JAK STAT pathway members, includ ing Jak1 and Stat1, were found to be upregulated in our study, suggesting that the JAK STAT pathway may be affected by bacterial infection, which may result in changes in other cross talk biological processes, such as NF B signaling selleck compound pathway, TGF b activated SMAD pathway, and apoptosis. Another signaling pathway affected by bacterial infec tion in the large yellow croaker was the MAPK cascade. This pathway has been demonstrated to regulate the expression of genes involved in the immune response to pathogens, cell differentiation, and cell death. Modulation of MAPK activity in the common periwin kle in response to Escherichia coli derived LPS has been studied. Some key MAPK related genes were identi fied in our transcriptome, including Casp9, Rac1, Gadd45a, and Dusp7.

Quantitative PCR analysis confirmed the differential expression of Casp9 and Dusp7. The Rho family GTPase Rac1 has been implicated in the control of the p38 MAPK signaling pathway by controlling b1 integrin. As shown in humans, dominant negative Rac1 completely inhibits b1 integrin induced p38 MAPK acti vation, whereas wild type Rac1 overexpression causes a slight increase in b1 integrin induced p38 MAPK activa tion. Dual specificity phosphatases including Dusp7 are a subset of protein tyrosine phosphatases, many of which dephosphorylate threonine and tyrosine residues on MAPKs and hence are also referred to as MAPK phosphatases. The regulated expression and activity of DUSP family members in different cells and tissues control MAPK intensity and duration to deter mine the type of physiological response.

There fore, the identified changes in gene expression in the large yellow croaker may facilitate the activation of the MAPK pathway and protect hosts against A. hydrophila infection. Adaptive immunity is the process that leads to specific host resistance to infection. T cells orchestrate responses against such foreign pathogens as viruses and bacteria. TCR and its downstream signaling cascades play a key role in these events. Here, we identified TCR pathway related genes that were downregulated at 24 h after A. hydrophila infection. This complex process is shown in Figure 4, and genes expressed differentially are listed in Additional file 7, Table S7.

Lyn, Itk, Was, Ptpn6, and Jun expression was downregulated, implying that the TCR signaling pathway may be suppressed in the early period following bacterial infection. Stu dies have shown that a fine balance exists between a positive signal that initiates TCR cascade Dacomitinib and a negative signal that controls the threshold, extent, and termina tion of TCR activation. Several protein tyrosine phosphatases have been shown to function as negative regulators of the TCR signaling pathway by dephosphorylating activated signaling molecules. Here, expression of Ptpn6, a member of the PTP family, was downregulated, suggesting that although the TCR signaling pathway was suppressed by A.