Intestinal inflammation is a primary contributor to poor growth performance during poultry production. Chlorogenic acid (CGA) is a natural phenolic acid that exhibits superior anti-inflammatory activity and improved intestinal health. To investigate the protective effects and molecular mechanisms of CGA during intestinal inflammation in lipopolysaccharide (LPS)-challenged broilers, we randomly divided 288 one-day-old male Cobb broilers into 4 groups: a control group fed a basal diet (CON group), a basal diet + LPS group (LPS group), and 2 basal diet groups fed 500 or 750 mg/kg CGA + LPS (CGA_{_500} or CGA_{_750} groups). Broilers were injected with LPS or saline at 15, 17, 19, and 21 d old. Chlorogenic acid supplementation improved the growth performance of LPS-challenged broilers by increasing average daily gain (ADG) and reducing feed/gain (F/G) ratios (P < 0.05). CGA also improved intestinal barrier function in LPS-challenged boilers by enhancing jejunum morphology and integrity, decreasing intestinal permeability, and increasing occludin 3, zonula occludens-1, and mucin 2 expression (P < 0.05). CGA supplementation also improved systemic and jejunum antioxidant capacity by significantly enhancing glutathione peroxidase (GSH-Px), superoxide dismutase (SOD), and catalase (CAT) activities (P < 0.05), and reducing malonaldehyde (MDA) and protein carbonyl (PCO) levels (P < 0.05). Chlorogenic acid supplementation reduced systemic and jejunum pro-inflammatory cytokines (interleukin (IL)-1β, IL-6, and IL-12) and increased anti-inflammatory cytokines (IL-10) in LPS-challenged broilers (P < 0.05) by inhibiting the toll like receptor 4 (TLR4)/nuclear factor kappa B (NF-κB) signaling pathway (P < 0.05). In addition, the protective effects of CGA toward intestinal inflammation and apoptosis appeared to be correlated with inhibited endoplasmic reticulum (ER) stress (P < 0.05). In summary, CGA supplementation improved intestinal morphology and integrity by inhibiting TLR4/NF-κB and ER stress pathways, which potentially reduced oxidative stress and inflammation, and ultimately improved the growth performance of LPS-challenged broilers.

The purpose of the study was to investigate the effects of Lactobacillus plantarum HW1 on growth performance, intestinal immune response, barrier function, and cecal microflora of broilers with necrotic enteritis. In total, 180 one-day-old male Cobb 500 broilers were randomly allocated into three groups comprising a non-infected control (NC) group, basal diet + necrotic enteritis challenge (NE) group, and basal diet + 4 × 10⁶ CFU/g Lactobacillus plantarum HW1 + necrotic enteritis challenge (HW1) group. Broilers in the NE and HW1 groups were orally given sporulated coccidian oocysts at day 14 and Clostridium perfringens from days 19 to 21. The results showed that the HW1 treatment increased (p < 0.05) the average daily gain of broilers from days 15 to 28 and from days 0 to 28 compared with the NE group. Moreover, the HW1 treatment decreased (p < 0.05) the oocysts per gram of excreta, intestinal lesion scores, ileal interleukin (IL) 1β and tumor necrosis factor α levels, and serum D-lactic acid and diamine oxidase levels, while increasing (p < 0.05) the ileal IL-10 level, thymus index, and protein expressions of ileal occludin and ZO-1. Additionally, the HW1 treatment decreased (p < 0.05) the jejunal and ileal villus height, jejunal villus height/crypt depth value, and cecal harmful bacterial counts (Clostridium perfringens, Salmonella, Escherichia coli, and Staphylococcus aureus), and increased (p < 0.05) the cecal Lactobacillus count. In conclusion, dietary supplementation with 4 × 10⁶ CFU/g Lactobacillus plantarum HW1 could relieve necrotic enteritis infection-induced intestinal injury and improve growth performance in broilers by improving intestinal barrier function and regulating intestinal microbiology.

The objective of this study is to investigate the beneficial effects and underlying mechanism of dietary β-mannanase supplementation on the productive performance of laying hens fed with metabolic energy (ME)-reduced diets. A total of 448 Hy-Line gray laying hens were randomly assigned to seven groups. Each group had 8 replicates with 8 hens. The groups included a control diet (CON) with a ME of 2750 kcal/Kg, diets reduced by 100 kcal/Kg or 200 kcal/Kg ME (ME_{_100} or ME_{_200}), and diets with 0.15 g/Kg or 0.2 g/Kg β-mannanase (ME_{_100}+β-M_{_0.15}, ME_{_100}+β-M_{_0.2}, ME_{_200}+β-M_{_0.15}, and ME_{_200}+β-M_{_0.2}). The productive performance, egg quality, intestinal morphology, inflammatory response, mRNA expression related to the Nuclear factor kappa B (NF-κB) and AMPK pathway, and cecum microbiome were evaluated in this study. ME-reduced diets negatively impacted the productive performance of laying hens. However, supplementation with β-mannanase improved FCR, decreased ADFI, and restored average egg weight to the level of the CON group. ME-reduced diets increased the levels of interleukin-1β (IL-1β) and IL-6 while decreasing the levels of IL-4 and IL-10 in the jejunum of laying hens. However, dietary β-mannanase supplementation improved jejunum morphology, reduced pro-inflammatory cytokine concentrations, and increased levels of anti-inflammatory factors in laying hens fed with ME-reduced diets. The mRNA levels of IL-6, IFN-γ, TLR4, MyD88, and NF-κB in the jejunum of ME-reduced diets were significantly higher than that in CON, dietary β-mannanase supplementation decreased these genes expression in laying hens fed with ME-reduced diets. Moreover, dietary β-mannanase supplementation also decreased the mRNA levels of AMPKα and AMPKγ, and increased the abundance of mTOR in the jejunum of laying hens fed with ME-reduced diets. Cecum microbiota analysis revealed that dietary β-mannanase increased the abundance of various beneficial bacteria (e.g., g_Pseudoflavonifractor, g_Butyricicoccus, and f_Lactobacillaceae) in laying hens fed with ME-reduced diets. In conclusion, dietary β-mannanase supplementation could improve the productive performance of laying hens fed with a ME-reduced diet by improving intestinal morphology, alleviating intestinal inflammation, changing energy metabolism-related signaling pathways, and increasing cecum-beneficial microbiota.

This study aimed to explore the effects of chili meal (CM), a by-product of chili pepper oil extraction, on the productive performance, intestinal health, and lipid metabolism of laying hens fed low-protein (LP) diets. A total of 384 Hy-Line brown laying hens (32 weeks old) were divided into six groups: control (CON) diet with 16.5 % crude protein (CP), LP diet with 15 % CP, and LP diets supplemented with 3 %, 5 %, 7 %, and 9 % CM. Results showed that dietary CM supplementation of up to 5 % did not negatively affect the productive performance of laying hens fed LP diets. However, the groups receiving 7 % and 9 % CM exhibited a significant increase in the feed-to-egg ratio (P < 0.05). Additionally, dietary CM supplementation effectively enhanced egg yolk color in a dose-dependent manner (P < 0.05). Intestinal morphology analysis indicated that the 5 % CM group had a higher villus height-to-crypt depth ratio than the LP and 9 % CM groups (P < 0.05), with no significant differences among the other groups. Dietary supplementation with 3 %-7 % CM did not significantly affect serum and jejunal antioxidant capacity, and the 9 % CM group exhibited the highest levels of serum and jejunal malondialdehyde among the groups (P < 0.05). Dietary CM supplementation significantly increased anti-inflammatory cytokines (IL-4 and IL-10) and decreased pro-inflammatory cytokines (IL-1β, IL-6, and TNF-α) in the serum and jejunal tissue of laying hens (P < 0.05). Moreover, CM supplementation significantly altered the cecal microbiota composition in laying hens, increasing the abundance of beneficial bacteria, such as Desulfovibrio and Megamonas. Furthermore, dietary CM supplementation significantly decreased serum triglyceride levels; downregulated liver mRNA levels of ACC, FAS, and SREBP-1C/2; and upregulated the mRNA levels of ACOX1, PPAR-α, Apob, and CPT in laying hens fed LP diets. In conclusion, CM supplementation should not exceed 5 % to avoid negative impacts on performance while supporting intestinal health and lipid metabolism.

Oxidative stress induces apoptosis and ferroptosis, leading to intestinal injury of piglets. Lactiplantibacillus plantarum P8 (P8) has antioxidant capacity, but its roles in intestinal apoptosis and ferroptosis remain unclear. Here, 24 weaned piglets were assigned to three treatments: control (Con), diquat injection (DQ), and P8 supplementation + DQ injection (DQ + P8). The results showed that the increased jejunal oxidative stress, jejunal morphology impairment, and barrier dysfunction in the DQ-treated piglets were decreased by P8 supplementation. TUNEL and apoptosis-related gene expressions showed increased jejunal apoptosis of DQ-treated piglets; however, reduced apoptosis was observed in the DQ + P8 group. In addition, the mitochondrial morphology and ferroptosis-related gene expressions indicated elevated jejunal ferroptosis in the DQ-treated piglets, and the DQ + P8 treatment attenuated the ferroptosis. Transcriptome identified various differentially expressed genes (DEGs) between different treatments. KEGG analysis indicated that the DEGs were enriched in the PI3K-AKT, NF-κB, and apoptosis pathways. The expressions of key DEGs and key proteins in the PI3K-AKT and NF-κB pathways were further verified. In summary, our results indicate that P8 supplementation ameliorated jejunal oxidative stress, morphological damage, barrier dysfunction, apoptosis, and ferroptosis in the DQ-treated piglets. Moreover, the beneficial effect of P8 may be related to the regulation of PI3K/AKT and NF-κB pathways.