Dataset Information

Trans-Anethole Alleviates Subclinical Necro-Haemorrhagic Enteritis-Induced Intestinal Barrier Dysfunction and Intestinal Inflammation in Broilers.

ABSTRACT: 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.

SUBMITTER: Yu C

PROVIDER: S-EPMC8977854 | biostudies-literature | 2022

REPOSITORIES: biostudies-literature

ACCESS DATA

Publications

Trans-Anethole Alleviates Subclinical Necro-Haemorrhagic Enteritis-Induced Intestinal Barrier Dysfunction and Intestinal Inflammation in Broilers.

Yu Caiyun C Wang Dong D Tong Yichun Y Li Qiming Q Yang Weiren W Wang Tian T Yang Zaibin Z

Frontiers in microbiology 20220321

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). Com ...[more]

PMID: 35387091

Similar Datasets

Project description: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.

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:BackgroundTransmissible gastroenteritis virus (TGEV) is one of the main pathogens causing severe diarrhea of piglets. The pathogenesis of TGEV is closely related to intestinal inflammation. All-trans retinoic acid (ATRA) is the main active metabolite of vitamin A, which has immunomodulatory and anti-inflammatory properties. However, it is unclear whether ATRA can alleviate TGEV-induced intestinal inflammation and barrier dysfunction in piglets. This study aimed to investigate the effects of ATRA on growth performance, diarrhea, intestinal inflammation and intestinal barrier integrity of TGEV-challenged piglets.MethodsIn a 19-d study, 32 weaned piglets were randomly divided into 4 treatments: Control group (basal diet), TGEV group (basal diet + TGEV challenge), TGEV + ATRA5 group (basal diet + 5 mg/d ATRA + TGEV challenge) and TGEV + ATRA15 group (basal diet + 15 mg/d ATRA + TGEV challenge). On d 14, piglets were orally administered TGEV or the sterile medium.ResultsFeeding piglets with 5 and 15 mg/d ATRA alleviated the growth inhibition and diarrhea induced by TGEV (P < 0.05). Feeding piglets with 5 and 15 mg/d ATRA also inhibited the increase of serum diamine oxidase (DAO) activity and the decrease of occludin and claudin-1 protein levels in jejunal mucosa induced by TGEV, and maintained intestinal barrier integrity (P < 0.05). Meanwhile, 5 mg/d ATRA feeding increased the sucrase activity and the expressions of nutrient transporter related genes (GLUT2 and SLC7A1) in jejunal mucosa of TGEV-challenged piglets (P < 0.05). Furthermore, 5 mg/d ATRA feeding attenuated TGEV-induced intestinal inflammatory response by inhibiting the release of interleukin (IL)-1β, IL-8 and tumor necrosis factor-α (TNF-α), and promoting the secretion of IL-10 and secretory immunoglobulin A (sIgA) (P < 0.05). Feeding 5 mg/d ATRA also down-regulated the expressions of Toll-like receptors and RIG-I like receptors signaling pathway related genes (TLR3, TLR4, RIG-I, MyD88, TRIF and MAVS) and the phosphorylation level of nuclear factor-κB-p65 (NF-κB p65), and up-regulated the inhibitor kappa B alpha (IκBα) protein level in jejunal mucosa of TGEV-challenged piglets (P < 0.05).ConclusionsATRA alleviated TGEV-induced intestinal barrier damage by inhibiting inflammatory response, thus improving the growth performance and inhibiting diarrhea of piglets. The mechanism was associated with the inhibition of NF-κB signaling pathway mediated by TLR3, TLR4 and RIG-I.

Project description:BackgroundSubclinical necrotic enteritis (SNE), a common intestinal disease of broiler caused by Clostridium perfringens, could reduce production performance of broilers by chronic intestinal damage and poor absorption of nutrients. Ellagic acid (EA) has been reported to present antioxidant and anti-inflammatory properties on human and animals in many aspects. This study was conducted to evaluate the effect and mechanism of EA in relieving SNE in broilers induced by C. perfringens.ResultsC. perfringens challenge decreased body weight (BW), average daily gain (ADG), jejunal villi height/crypt depth (V/C) ratio, the activity of catalase (CAT) and the mRNA expression of zonula occludens 1 (ZO-1) in jejunal mucosa of broilers. While feed conversion ratios (FCR), jejunal crypt depth (CD), the activities of myeloperoxidase (MPO) and diamine oxidase (DAO), as well as the concentrations of interleukin 6 (IL-6), C-reactive protein (CRP) and procalcitonin (PCT) in serum, the activities of inducible nitric oxide synthase (iNOS) and lysozyme (LZM), the concentration of malondialdehyde (MDA), and the mRNA expressions of claudin-2, TNF-α, IL-1β, TLR-4, TLR-2, NF-κB, JAK3, STAT6 and iNOS in jejunal mucosa of broilers were increased by C. perfringens challenge. Dietary EA supplement relieved these adverse effects, and heightened jejunal villi height (VH), the concentration of D-xylose in plasma, activity of superoxide dismutase (SOD), and the mRNA expression of occludin in jejunal mucosa of broilers. The alpha diversity of cecal microbiota indicated that dietary EA supplement increased observed species and Shannon index. C. perfringens challenge increased the relative abundance of Firmicutes and decreased the relative abundance of Desulfobacterota in cecal microbiota. EA increased the relative abundance of Firmicutes in cecal microbiota. LEfSe analysis showed that C. perfringens challenge triggered the imbalance of cecal microbiota in broilers, dietary EA supplementation led to a small beneficial effect on microbiota, while the simultaneous effect of them seemed to stimulate the immune function of broilers by improving the microbiota balance.ConclusionsDietary EA ameliorated C. perfringens-induced SNE in broilers via regulating jejunal inflammation signaling pathways TLR/NF-κB and JAK3/STAT6, relieving jejunal oxidative stress and balancing cecal microbiota to inhibit intestinal barrier damage, prevent systemic inflammatory response and improve nutrient absorption capacity, finally protect and enhance growth performance of broilers.

Dataset Information

Trans-Anethole Alleviates Subclinical Necro-Haemorrhagic Enteritis-Induced Intestinal Barrier Dysfunction and Intestinal Inflammation in Broilers.

Publications

<i>Trans</i>-Anethole Alleviates Subclinical Necro-Haemorrhagic Enteritis-Induced Intestinal Barrier Dysfunction and Intestinal Inflammation in Broilers.

Similar Datasets

OmicsDI is part of the ELIXIR infrastructure

Tweets