Chlorogenic acids (CGA) are widely used as feed additives for their ability to improve growth performance and intestinal health in poultry. However, whether dietary CGAs could reverse the impaired intestinal condition caused by high stocking density (HD) in broiler chickens is unknown. We determined the effect of dietary CGA on growth, serum antioxidant levels, jejunum barrier function, and the microbial community in the cecum of broilers raised under normal (ND) or HD conditions. HD stress significantly decreased growth and body weight, which was restored by CGA. The HD group showed increased serum malondialdehyde, an oxidative byproduct, and decreased SOD and GSH-Px activity. CGA reduced malondialdehyde and restored antioxidant enzyme activity. HD stress also significantly decreased jejunal villus length and increased crypt depth. Compared with ND, the expression of tight-junction genes was significantly decreased in the HD group, but this decrease was reversed by CGA. HD also significantly upregulated TNF-α. Compared with ND, the cecal microbiota in the HD group showed lower alpha diversity with increases in the harmful bacteria Turicibacter and Shigella. This change was altered in the HD + CGA group, with enrichment of Blautia, Akkermansia, and other beneficial bacteria. These results demonstrated that HD stress decreased serum antioxidant capacity, inhibited the development of jejunal villi, and downregulated expression of tight-junction genes, which increased intestinal permeability during the rapid growth period (21 to 35 days). Dietary CGA enhanced antioxidant capacity, improved intestinal integrity, and enhanced beneficial gut bacteria in chickens raised under HD conditions.

The study was conducted to evaluate the effects of dietary chlorogenic acid supplementation on the growth performance, antioxidant function, and immune response of broiler breeders exposed to immune stress or high stocking density stress. The test was divided into two stress models. For the immune stress test, 198 birds were distributed into three experimental treatments with six replicates per treatment. The treatments were: (1) saline control (birds injected with saline and fed basal diet), (2) LPS group (birds injected with 0.5 mg LPS/kg body weight and fed basal diet), and (3) CGA + LPS group (birds injected with LPS and fed basal diet supplemented with 1 g/kg CGA. LPS was intraperitoneally injected from day 14, and then daily for 10 days. For the high stocking density stress model, 174 birds were distributed into three experimental treatments with six replicates per treatment. The treatments were: (1) controls (birds fed basal diet and raised at a stocking density of 14 broilers per m²), (2) high-density group (birds fed with basal diet and raised at a stocking density of 22 broilers per m²), and (3) high density + CGA group (birds fed with 1 g/kg CGA and raised at a stocking density of 22 broilers per m²). Results showed that LPS injection and high stocking density significantly decreased the body weight and feed intake of broiler breeders, while CGA supplementation increased feed intake of broiler breeders under LPS injection and high stocking density stress. Moreover, LPS injection and high stocking density increased the concentration of corticosterone in serum, and CGA addition remarkably downregulated serum corticosterone levels. The GSH level decreased with LPS injection and CGA increased the GSH concentration in the intestines of immune-stressed broiler breeders. LPS injection promoted the production of circulating proinflammatory cytokines (serum IL-1β and TNF-α) by 72 h after LPS injection. Dietary supplementation with CGA prevented the increase in serum TNF-α caused by LPS. These results suggest that dietary inclusion of 1 g/kg CGA could increase the feed intake of broiler breeders and alleviate the effects of inflammatory mediator stress and exposure to high stocking density.

Objective. This study investigated the nature of shared transcriptomic alterations in PBMs from periodontitis and atherosclerosis to unravel molecular mechanisms underpinning their association. Methods. Gene expression data from PBMs from patients with periodontitis and those with atherosclerosis were each downloaded from the GEO database. Differentially expressed genes (DEGs) in periodontitis and atherosclerosis were identified through differential gene expression analysis. The disease-related known genes related to periodontitis and atherosclerosis each were downloaded from the DisGeNET database. A Venn diagram was constructed to identify crosstalk genes from four categories: DEGs expressed in periodontitis, periodontitis-related known genes, DEGs expressed in atherosclerosis, and atherosclerosis-related known genes. A weighted gene coexpression network analysis (WGCNA) was performed to identify significant coexpression modules, and then, coexpressed gene interaction networks belonging to each significant module were constructed to identify the core crosstalk genes. Results. Functional enrichment analysis of significant modules obtained by WGCNA analysis showed that several pathways might play the critical crosstalk role in linking both diseases, including bacterial invasion of epithelial cells, platelet activation, and Mitogen-Activated Protein Kinases (MAPK) signaling. By constructing the gene interaction network of significant modules, the core crosstalk genes in each module were identified and included: for GSE23746 dataset, RASGRP2 in the blue module and VAMP7 and SNX3 in the green module, as well as HMGB1 and SUMO1 in the turquoise module were identified; for GSE61490 dataset, SEC61G, PSMB2, SELPLG, and FIBP in the turquoise module were identified. Conclusion. Exploration of available transcriptomic datasets revealed core crosstalk genes (RASGRP2, VAMP7, SNX3, HMGB1, SUMO1, SEC61G, PSMB2, SELPLG, and FIBP) and significant pathways (bacterial invasion of epithelial cells, platelet activation, and MAPK signaling) as top candidate molecular linkage mechanisms between atherosclerosis and periodontitis.

Broilers grown in a high-density (HD) stocking environment may experience intense competition that may adversely affect their growth relative to animals reared at a normal density (ND). The growth performance of HD broilers is increased by aspirin eugenol ester (AEE), although the mechanism by which this compound modulates hypothalamus-regulated feeding behavior is unclear. The aims of this study were to determine the effects of including AEE in the basal diet on the hypothalamic transcriptome and to examine in parallel the impact of these modifications on broiler production performance in HD conditions. Three hundred sixty one-day-old male Arbor Acres broilers were randomly divided into four groups: an ND group (14 broilers/m²), HD group (22 broilers/m²), ND-AEE group, and HD-AEE group. Each treatment group had 10 replicates, with 7 broilers per replicate in the ND and ND-AEE groups and 11 broilers per replicate in the HD and HD-AEE groups. Broiler growth performance was monitored, and hypothalamus samples were collected for transcriptome analysis on day 28. The HD group exhibited a reduced body weight (p < 0.01) at this timepoint compared to the ND group. However, the addition of AEE significantly improved average daily feed intake, average daily gain, and feed conversion ratio in the HD group from days 22 to 28 compared to the HD group without AEE (p < 0.05). The transcriptome results showed that 20 signaling pathways were commonly enriched among the groups (ND vs. HD, HD vs. HD-AEE). Several potential candidate genes were identified as involved in chicken central nervous system development and regulation of feed intake. Thus, the current study provides new insights into hypothalamic transcription patterns that are associated with the ameliorative effects of AEE in HD broilers.

Immune stress in broilers can cause severe economic losses, and chlorogenic acid (CGA) is an effective plant extract for alleviating immune stress. This study investigated the effects of CGA on the intestinal microbiota and metabolites of broilers under immune stress. A group of 312 broiler chicks was randomly divided into four treatment groups: Saline control, lipopolysaccharide (LPS), LPS + CGA (LCGA), and Saline + CGA (SCGA). The SCGA and LCGA groups were fed a basal diet supplemented with 1,000 mg/kg CGA throughout the whole experimental period. The LPS and LCGA groups were injected with 0.5 mg/kg LPS on days 14, 15, and 16 to induce immune stress. At day 17, the ileal contents were collected for analysis. Results showed that LPS-induced immune stress decreased the abundance of Subdoligranulum , thereby lowering microbial richness. However, dietary CGA increased beneficial bacteria like Clostridiaceae ( P < 0.05) and Candidatus Arthromitus ( P < 0.01) in immune-stressed broilers, while reducing harmful Lachnospiraceae ( P < 0.05) and Desulfovibrionaceae ( P < 0.05). Non-targeted metabolomics revealed that immune stress significantly increased methylmalonic acid, N-acetyl-L-aspartic acid, trans-ferulic acid, and pantothenic acid, while significantly downregulating pyroglutamic acid, L-glutamic gamma-semialdehyde, and biliverdin, indicating that immune stress (LPS) induced inflammation and oxidative damage. CGA addition reduced corticosterone, prostaglandin B2, trans-ferulic acid, and methylmalonic acid levels, while increasing pyroglutamic acid, L-glutamic gamma-semialdehyde, biliverdin, chenodeoxycholic acid, desmosterol, and 4-hydroxycinnamic acid, confirming that CGA can alleviate inflammation and enhance antioxidant capacity by influencing ileal microbiota and specific metabolite synthesis. IMPORTANCE: Our previous research indicated that CGA could effectively alleviate immune stress in broilers. However, it was unclear whether its antistress effects were achieved by altering the gut microbiota and metabolites in the ileum of immune-stressed broilers. In this study, CGA altered gut microbiota and metabolites associated with alleviating immune stress were provided, which will provide new insights into strategies to target gut microbiota and metabolites to relieve immune stress in broilers. These findings contribute to a better understanding of the mechanism of action of CGA on the attenuation of immune stress and provide new approaches to immune stress therapy by regulating gut microbiota and metabolites.