Dataset Information

Probiotic Enhanced Intestinal Immunity in Broilers against Subclinical Necrotic Enteritis.

ABSTRACT: Along with banning of antibiotics, necrotic enteritis (NE), especially subclinical NE (SNE) whereby no clinical signs are present in chicks, has become one of the most threatening problems in poultry industry. Therefore, increasing attention has been focused on research and application of effective probiotic strains, as an alternative to antibiotics, to prevent SNE in broilers. In the present study, we evaluated the effects of Lactobacillus johnsonii BS15 on the prevention of SNE in broilers. Specifically, assessment determined the growth performance and indexes related to intestinal mucosal immunity in the ileum and cecal tonsil of broilers. A total of 300 1-day-old Cobb 500 chicks were randomly distributed into the following 5 groups: control group (fed with basal diet?+?de Man, Rogosa, and Sharpe liquid medium [normal diet]), SNE group (normal diet), BS15 group (basal diet?+?1?×?106 colony-forming units BS15/g as fed [BS15 diet]), treatment group (normal diet [days 1-28]?+?BS15 diet [days 29-42]), and prevention group (BS15 diet [days 1-28]?+?normal diet [days 29-42]) throughout a 42-day experimental period. SNE infection was treated for all chicks in the SNE, BS15, treatment, and prevention groups. The present results demonstrated that BS15 supplementation of feeds in BS15 and prevention groups exerted a positive effect on preventing negative influences on growth performance; these negative influences included low body weight gain and increased feed conversion ratio caused by SNE. Although no changes were detected in all determined indexes in cecal tonsils, BS15-treated broilers were free from SNE-caused damage in villi in the ileum. BS15 inhibited SNE-caused decrease in immunoglobulins in the ileum. In the lamina propria of ileum, T cell subsets of lymphocytes influenced by SNE were also controlled by BS15. BS15 affected antioxidant abilities of the ileum and controlled SNE-induced mitochondrion-mediated apoptosis by positively changing contents and/or mRNA expression levels of apoptosis-related proteins. These findings indicate that BS15 supplementation may prevent SNE-affected growth decline mainly through enhancing intestinal immunity in broilers.

SUBMITTER: Wang H

PROVIDER: S-EPMC5701917 | biostudies-literature | 2017

REPOSITORIES: biostudies-literature

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Probiotic Enhanced Intestinal Immunity in Broilers against Subclinical Necrotic Enteritis.

Wang Hesong H Ni Xueqin X Qing Xiaodan X Liu Lei L Lai Jing J Khalique Abdul A Li Guangyao G Pan Kangcheng K Jing Bo B Zeng Dong D

Frontiers in immunology 20171120

Along with banning of antibiotics, necrotic enteritis (NE), especially subclinical NE (SNE) whereby no clinical signs are present in chicks, has become one of the most threatening problems in poultry industry. Therefore, increasing attention has been focused on research and application of effective probiotic strains, as an alternative to antibiotics, to prevent SNE in broilers. In the present study, we evaluated the effects of <i>Lactobacillus johnsonii</i> BS15 on the prevention of SNE in broil ...[more]

PMID: 29209325

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Project description:Necrotic enteritis infection poses a serious threat to poultry production, and there is an urgent need for searching effective antibiotic alternatives to control it with the global ban on in-feed antibiotics. This study was conducted to investigate the effects of dietary Bacillus licheniformis replacing enramycin on the growth performance and intestinal health of subclinical necrotic enteritis (SNE)-challenged broilers. In total, 504 1-day-old Arbor Acres male chickens were selected and subsequently assigned into three treatments, including PC (basal diet + SNE challenge), PA (basal diet extra 10 mg/kg enramycin + SNE challenge), and PG (basal diet extra 3.20 × 109 and 1.60 × 109 CFU B. licheniformis per kg diet during 1-21 days and 22-42 days, respectively + SNE challenge). Results showed that B. licheniformis significantly decreased the intestinal lesion scores and down-regulated the Claudin-3 mRNA levels in jejunum of SNE-infected broilers on day 25, but increased the mucin-2 gene expression in broilers on day 42. In addition, B. licheniformis significantly up-regulated the mRNA levels of TRIF and NF-κB of SNE-challenged broilers compared with the control group on day 25 and TLR-4, TRIF compared with the control and the antibiotic group on day 42. The mRNA expression of growth factors (GLP-2 and TGF-β2) and HSPs (HSP60, HSP70, and HSP90) were up-regulated in B. licheniformis supplementary group on days 25 and 42 compared with group PC. LEfSe analysis showed that the relative abundance of Lachnospiraceae_UCG_010 was enriched in the PG group; nevertheless, Clostridiales_vadinBB60 and Rnminococcaceae_NK4A214 were in PA. PICRUSt analysis found that the metabolism of cofactors and vitamins, amino acid metabolism, and carbohydrate metabolism pathways were enriched, whereas energy metabolism, membrane transport, cell motility, and lipid metabolism were suppressed in B. licheniformis-supplemented groups as compared with the PC control. In conclusion, dietary supplementation of B. licheniformis alleviated the intestinal damage caused by SNE challenge that coincided with modulating intestinal microflora structure and barrier function as well as regulating intestinal mucosal immune responses.

Project description:This study aimed to determine the effects of chlorogenic acid (CGA) on the growth performance, intestinal health, immune response, and mitochondrial DNA (mtDNA)-cyclic GMP-AMP synthase (cGAS)-stimulator of interferon genes (STING) signaling pathway in broilers under necrotic enteritis (NE) challenge. The 180 one-day-old male Cobb 500 broilers with similar body weight of 44.59 ± 1.39 g were randomly allocated into 3 groups. The groups were control diet (Control group), control diet + NE challenge (NE group), and control diet + 500 mg/kg CGA + NE challenge (NE + CGA group), with 6 replicates per treatment. All broilers except the Control group were given sporulated coccidian oocysts (d 14) and Clostridium perfringens (d 19-21) by oral gavage. Our findings showed that CGA improved the growth performance and intestinal morphology in broilers under NE challenge. CGA supplementation elevated the barrier function in broilers under NE challenge, which reflected in the decreased serum concentrations of D-lactate and diamine oxidase, and upregulated jejunal protein expression of occludin. CGA supplementation also improved the immune function, which reflected in the increased concentrations and gene expressions of anti-inflammatory factors, and decreased concentrations and gene expressions of proinflammatory factors. CGA supplementation further enhanced intestinal cell proliferation and differentiation, which manifested in the increased number of goblet cells and positive cells of proliferating cell nuclear antigen on d 28 and 42. Furthermore, CGA supplementation decreased the mtDNA (d 42) and mitochondrial reactive oxygen species levels (d 28 and 42), and increased the mitochondrial membrane potential (d 42) and mitochondrial complex I (d 28 and 42) or III (d 28) activity. Broilers challenged with NE had upregulated jejunal protein expressions of cGAS, phospho-TANK-binding kinase 1, and phospho-interferon regulatory factor 7 compared with the Control group, which were downregulated after CGA supplementation. In conclusion, dietary supplementation CGA could protect against intestinal inflammation and injury by reducing the leakage of mtDNA and inactivating the cGAS-STING signaling pathway in broilers under NE challenge.

Project description:This study investigated the alleviative potential of trans-anethole (TA) on the impaired intestinal barrier and intestinal inflammation and its regulatory effects on gut microbiota in broilers with subclinical necro-hemorrhagic enteritis (NE) challenge. Subclinical NE challenge led to a severe decline in the 21-day body weight (BW) and average daily gain (ADG), but an increase in feed conversion ratio (FCR) and intestinal lesion score of birds compared with controls (P < 0.05). Compared with the subclinical NE group, the TA administration group exhibited lower (P < 0.05) intestinal lesion score and crypt depth (CD), serum diamine oxidase activity, and D-lactate concentration, but higher (P < 0.05) intestinal tight junction protein expressions, villus height (VH), VH/CD, and numbers of proliferating cell nuclear antigen (PCNA)-positive cells. The administration of TA also inhibited (P < 0.05) the expression of intestinal pro-inflammatory cytokines including interleukin (IL)-1β, IL-8, interferon-gamma (IFN-γ), and tumor necrosis factor-alpha (TNF-α) but increased (P < 0.05) jejunal IL-10 and secretory immunoglobulin A (sIgA) concentration. TA inclusion also led to a remarkable reduction of intestinal NF-kappa-B inhibitor alpha (IκBα) degradation and nuclear factor kappa beta (NF-κB) translocation. Moreover, TA modulated the cecal microbiota abundance and diversity of NE birds, as confirmed by reducing the phylum Firmicutes and genera Ruminococcaceae_UCG-014, Eubacterium_coprostanoligenes_group, and Ruminococcaceae_NK4A214_group when supplemented at 600 mg/kg and reducing genera Butyricicoccus, Oscillibacter, and Flavonifractor when supplemented at 400 mg/kg (P < 0.05). Supplementation of TA in broiler diets could alleviate subclinical NE infection by restoring intestinal barrier integrity, inhibiting NF-κB signaling pathway, and modulating gut microbiota. A 600-mg/kg dose of TA is the optimum concentration for ameliorating subclinical NE in broilers.

Project description:The dysfunction of tight-junction integrity caused by necrotic enteritis (NE) is associated with decreased nutrient absorption and gut injury in broiler chickens. Although probiotic Enterococcus faecium (E. faecium) has been reported to possess immune-regulatory characteristics and can prevent diarrhea in pigs, very little information exists in relation to the specific regulatory impact of E. faecium NCIMB 11181 on NE-induced intestinal barrier injury of broiler chickens. This study was conducted to investigate the protective effects of probiotic E. faecium NCIMB 11181 on NE-induced intestinal barrier injury in broiler chickens. The study also aimed to elucidate the mechanisms that underpin these protective effects. One hundred and eighty Arbor Acres (AA) broiler chicks (one day old) were randomly assigned using a 2 × 2 factorial arrangement into two groups fed different levels of dietary E. faecium NCIMB 11181 (0 or 2 × 108 CFU/kg of diet) and two disease-challenge groups (control or NE challenged). The results showed that NE induced body weight loss, intestinal lesions, and histopathological inflammation, as well as intestinal-cell apoptosis. These symptoms were alleviated following the administration of probiotic E. faecium NCIMB 11181. Pretreatment with probiotic E. faecium NCIMB 11181 significantly upregulated the expression of the Claudin-1 gene encoding a tight-junction protein. Claudin-1 and HSP70 protein expression were also increased in the jejunum regardless of NE infection. Furthermore, NE-infected birds fed with E. faecium displayed notable increases in MyD88, NF-κB, iNOS, PI3K, GLP-2, IL-1β, IL-4, and HSP70 mRNA expression. E. faecium NCIMB 11181 administration also significantly improved the animals' intestinal microbial composition regardless of NE treatment. These findings indicated that addition of E. faecium NCIMB 11181 to poultry feed is effective in mitigating NE-induced gut injury, possibly by strengthening intestinal mucosal barrier function, as well as modulating gut microflora and intestinal mucosal immune responses.

Dataset Information

Probiotic Enhanced Intestinal Immunity in Broilers against Subclinical Necrotic Enteritis.

Publications

Probiotic Enhanced Intestinal Immunity in Broilers against Subclinical Necrotic Enteritis.

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