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The excessive deposition of abdominal adipocytes in chickens is detrimental to poultry production. However, the regulatory factors that affect abdominal adipogenesis in chickens are still poorly understood. SLC22A16 is differentially expressed in abdominal preadipocytes and 10-day differentiated adipocytes in chickens, but its role in regulating chicken adipogenesis has not been reported. In this study, the function of SLC22A16 in chicken abdominal preadipocytes was investigated. SLC22A16 is significantly upregulated during abdominal adipocyte differentiation. The overexpression of SLC2A16 upregulated the expression of adipogenic marker genes and proliferation-related genes, and promoted the proliferation of adipocytes and the accumulation of triglycerides. The knockdown of SLC22A16 downregulated the expression of adipogenic marker genes and proliferation-related genes, inhibited the proliferation of adipocytes, and impaired the accumulation of triglycerides in adipocytes. In addition, LNC6302 was differentially expressed in abdominal preadipocytes and mature adipocytes, and was significantly positively correlated with the expression of SLC22A16. Interference with LNC6302 inhibits the expression of adipogenic marker genes and proliferation-related genes. The data supported the notion that LNC6302 promotes the differentiation of chicken abdominal adipocytes by cis-regulating the expression of SLC22A16. This study identified the role of SLC22A16 in the differentiation and proliferation of chicken adipocytes, providing a potential target for improving abdominal adipogenesis in chickens. [ABSTRACT FROM AUTHOR]

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 p-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—CXCL13L2, CSF3R, CSF2RB, CCR9, CCR10, IL1R1, IL8L1, IL8L2, GHR, KIT, OSMR, TNFRSF13B, TNFSF13B, and TGFBR2L. At the same time, immune-related SDEGs including CCR9, CCR10, DMB1, TNFRSF13B, TNFRSF13C and TNFSF13B were significantly enriched in the intestinal immune network for the IgA production signaling pathway. The SDEG protein-protein interaction module analysis showed that CXCR5, CCR8L, CCR9, CCR10, IL8L2, IL8L1, TNFSF13B, TNFRSF13B and TNFRSF13C 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. [ABSTRACT FROM AUTHOR]