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.

Fasting-induced molting (FIM) is a common method used to improve the laying performance of aged laying hens. Nevertheless, this approach may impose various stresses on chickens, such as disruptions in intestinal flora and inflammation issues within the intestines. However, the impact of an imbalance in intestinal flora on intestinal health during the FIM process remains elusive. Therefore, intestinal injury, the microbiome, and the metabolome were analyzed individually and integrated to elucidate the impact of the intestinal flora on intestinal health during the FIM process. The findings indicated that fasting resulted in a notable reduction in villus height and villus/crypt ratio, coupled with elevated levels of intestinal inflammation and permeability. During the fasting period, microbiota compositions changed. The abundance of Escherichia_Shigella increased, while the abundance of Ruminococcaceae_UCG-013 and Lactobacillus decreased. Escherichia_Shigella was positively correlated with Citrinin and Sterobilin, which lead to intestinal inflammation. Ruminococcaceae_UCG-013 and Lactobacillus exhibited positive correlations with Lanthionine and reduced Glutathione, thereby reducing intestinal inflammation. This study screened the intestinal probiotics, Ruminococcaceae UCG-013 and Lactobacillus, that influence gut health during the fasting period, providing an experimental basis for improving gut microbiota and reducing intestinal inflammation during the FIM process.

This study investigated the effects of dietary supplementation with Vitamin E (VE) and selenium (Se) on immunostressed broilers. In the experiment, a total of 576 Gushi chickens were randomly allocated into 12 groups. They were respectively fed diets with different levels of VE and Se. Lipopolysaccharide (LPS) immune treatment was administered at 23, 25, and 27 days of age. At 28 days of age, the antioxidant indicators and immune factors in their serum, liver, and intestine were measured. The results indicated that (1) LPS treatment significantly elevated the contents of nitric oxide (NO) and nitric oxide synthase (NOS) in the duodenum and jejunum (p < 0.01). Conversely, adding VE and Se to the diet of LPS-treated chicks could significantly decrease the content of NO in the duodenum and the activities of NOS in the duodenum and jejunum (p < 0.01). (2) LPS treatment significantly decreased the content of malondialdehyde (MDA) in the liver of broilers, glutathione peroxidase (GSH-Px), and the activities of serum superoxide dismutase (SOD) (p < 0.01). Dietary supplementation of selenium could significantly reduce the content of MDA (p < 0.01), and the treatment groups with 200 mg/kg VE and 0.6 mg/kg Se exhibited the most favorable effects. (3) Adding Se or VE to the diet of LPS-treated chicks could significantly increase the thymus index and spleen index (p < 0.05) and significantly decrease the bursa of Fabricius index (p < 0.05). Among them, the thymus index was the highest in the 100 mg/kg VE group, and the interaction of the three factors had a significant influence on the thymus index and bursa of Fabricius index (p < 0.05). (4) The level ofinterleukin-6 (IL-6) in the serum of broilers in the LPS treatment group was significantly increased. However, selenium and Vitamin E were added to the diet of LPS-treated chicks to reduce the contents of serum IL-6 and IL-8, as well as adrenocorticotropic hormone (ACTH) and tumor necrosis factor-α (TNF-α). Moreover, the interaction of the three factors has a significant impact on immune indicators (p < 0.01). In conclusion, adding 100–200 mg/kg of VE and 0.6 mg/kg of Se to the diet of broiler chickens has certain advantages in enhancing immunity and antioxidant capacity.

High-temperature environments induce heat stress in poultry, leading to compromised immune function and reduced disease resistance. In the Dexamethasone-induced stress-related immune suppression model in chickens, both transcriptomic and proteomic analyses revealed significantly low expression of GBP4L, highlighting its potential as a key target for combating stress. It is currently unclear whether GBP4L can alleviate the heat stress response in the body. We conducted this study to explore the role of GBP4L in stress resistance. First, to evaluate the role of GBP4L in immune function, we established an inflammatory cell model via Lipopolysaccharide (LPS) treatment and then generated both a pcDNA3.1-EGFP-GBP4L plasmid and a si-GBP4L interference fragment for transfection into HD11 model cells. Next, we exposed 28-day-old Gushi roosters to high heat (32 ± 1 °C) for 4 weeks to establish a heat stress model. We administered a virus carrying pAAV-GBP4L-3FLAG via subcutaneous injection, evaluated immune marker levels and conducted ATAC-seq on spleen tissues to investigate the effect of GBP4L on chromatin accessibility. The results revealed that GBP4L overexpression reduced the expression of proinflammatory factors, promoted the polarization of HD11 cells from the M1 phenotype to the M2 phenotype, reduced the LPS-induced expression of IL-8 (P < 0.05), alleviated inflammation, increased cell proliferation (P < 0.05), and inhibited apoptosis (P < 0.05). In the animal model, increasing the expression of GBP4L alleviated heat stress-induced inflammation, improved blood biochemistry, enhanced immune function in the spleen and bursa of Fabricius, and preserved the structure of the spleen. ATAC-seq revealed that GBP4L reduced chromatin accessibility in the promoter regions of 34 heat stress-induced genes. Furthermore, the expression of SP9 was significantly increased in animals under heat stress but was decreased in animals overexpressing GBP4L under heat stress. In conclusion, GBP4L alleviates heat stress-induced inflammation, enhances immune status, and reduces spleen tissue damage. Mechanistically, GBP4L overexpression may enhance heat stress resistance by altering chromatin spatial structure to regulate SP9 expression. The research findings offer valuable insights into the mechanisms of heat stress resistance in poultry, contributing to the development of strategies to enhance heat tolerance. These results also expand the epigenetic regulation theory of heat tolerance and support the breeding of heat-tolerant chicken varieties.