| Summary: | Stress-induced immunosuppression is a common problem in the poultry industry, but the specific mechanism of its effect on the immune function of chicken has not been clarified. In this study, 7-day-old Gushi cocks were selected as subjects, and a stress-induced immunosuppression model was successfully established via daily injection of 2.0 mg/kg (body weight) dexamethasone. We characterized the spleen transcriptome in the control (B_S) and model (D_S) groups, and 515 significant differentially expressed genes (SDEGs) (Fragments Per Kilobase of transcript sequence per Millions base pairs sequenced (FPKM) > 1, adjusted <i>p</i>-value (padj) < 0.05 and Fold change (|FC|) ≥ 2) were identified. The cytokine-cytokine receptor interaction signaling pathway was identified as being highly activated during stress-induced immunosuppression, including the following SDEGs—<i>CXCL13L2, CSF3R, CSF2RB, CCR9, CCR10, IL1R1, IL8L1, IL8L2, GHR, KIT, OSMR, TNFRSF13B, TNFSF13B</i>, and <i>TGFBR2L</i>. At the same time, immune-related SDEGs including <i>CCR9</i>, <i>CCR10, DMB1, TNFRSF13B, TNFRSF13C </i>and<i> TNFSF13B</i> were significantly enriched in the intestinal immune network for the IgA production signaling pathway. The SDEG protein-protein interaction module analysis showed that <i>CXCR5, CCR8L, CCR9, CCR10, IL8L2, IL8L1, TNFSF13B, TNFRSF13B</i> and <i>TNFRSF13C</i> may play an important role in stress-induced immunosuppression. These findings provide a background for further research on stress-induced immunosuppression. Thus, we can better understand the molecular genetic mechanism of chicken stress-induced immunosuppression.
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