Dataset Information

Bacillus licheniformis normalize the ileum microbiota of chickens infected with necrotic enteritis.

ABSTRACT: Necrotic enteritis (NE) is a severe intestinal disease, which can change gut microbiota and result in a high cost for the poultry industry worldwide. However, little is known regarding how the gut microbiota of NE chicken ileum are changed by Bacillus licheniformis. This study was conducted to investigate how ileum microbiota structure was changed by B. licheniformis in broiler chickens challenged with Clostridium perfringens-induced NE through Illumina MiSeq sequencing. The broilers were randomly separated into four groups: the negative control group (NC), the positive control group (PC), the fishmeal and coccidia group (FC), and the PC group supplied with feed containing B. licheniformis (BL). Compared to the PC and FC, alpha diversity, beta diversity, and the bacterial taxa of the ileum microbiota were more similar in BL and NC. Some genera, which were related to the NE control, became insignificant in BL with NC, such as Lactobacillus, Lactococcus, Bacteroides, Ruminococcus and Helicobacter. The PICRUSt analysis revealed that a tumour suppressor gene, p53, which was negatively correlated with Helicobacter, was enriched in the BL group. Our findings showed that the ileum microbiota disorder caused by NE in chickens was normalized by dietary B. licheniformis supplementation.

SUBMITTER: Xu S

PROVIDER: S-EPMC5789067 | biostudies-literature | 2018 Jan

REPOSITORIES: biostudies-literature

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Bacillus licheniformis normalize the ileum microbiota of chickens infected with necrotic enteritis.

Xu Shuai S Lin Yicen Y Zeng Dong D Zhou Mengjia M Zeng Yan Y Wang Hesong H Zhou Yi Y Zhu Hui H Pan Kangcheng K Jing Bo B Ni Xueqin X

Scientific reports 20180129 1

Necrotic enteritis (NE) is a severe intestinal disease, which can change gut microbiota and result in a high cost for the poultry industry worldwide. However, little is known regarding how the gut microbiota of NE chicken ileum are changed by Bacillus licheniformis. This study was conducted to investigate how ileum microbiota structure was changed by B. licheniformis in broiler chickens challenged with Clostridium perfringens-induced NE through Illumina MiSeq sequencing. The broilers were random ...[more]

PMID: 29379124

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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:BackgroundIntestinal microbiota is critical for maintaining animal health and homeostasis. However, involvement of the fungal community, also known as the mycobiota, in animal health and disease is poorly understood. This study was aimed to examine the association between the intestinal mycobiota and the severity of necrotic enteritis (NE), an economically significant poultry disease.MethodsA total of 90 day-of-hatch Cobb broilers were infected with Eimeria maxima on d 10, followed by an oral challenge with C. perfringens on d 14 to induce NE, while another 10 broilers were served as mock-infected controls. On d 17, the lesions in the jejunum were scored, and the ileal digesta were subjected to DNA isolation and real-time PCR quantification of total bacterial and fungi populations. Internal transcribed spacer 2 (ITS2) amplicon sequencing was also performed to profile the ileal mycobiota composition. Changes in the ileal mycobiota in response to NE were investigated. Spearman correlation analysis was further conducted to identify the correlations between relative abundances of individual ileal fungi and the severity of NE.ResultsWhile the total bacterial population in the ileum was increased by 2- to 3-fold in NE chickens, the total fungal population was progressively declined in more exacerbated NE, with the most severely infected chickens showing a nearly 50-fold reduction relative to mock-infected controls. Richness of the ileal mycobiota also tended to reduce in chickens with NE (P = 0.06). Compositionally, among 30 most abundant fungal amplicon sequence variants (ASVs), 11 were diminished and 7 were enriched (P < 0.05), while 12 remained largely unchanged in NE-afflicted chickens (P > 0.05). Multiple Wallemia and Aspergillus species were markedly diminished in NE (P < 0.05) and also showed a significant negative correlation with NE severity (P < 0.05).ConclusionsDysbiosis of the ileal mycobiota is induced evidently by NE and the extent of the dysbiosis is positively correlated with disease severity. These findings suggest a possible role of the intestinal mycobiota in NE pathogenesis and highlight the mycobiota as a new potential target for NE mitigation in poultry.

Project description:Background:Clostridium perfringens-induced chicken necrotic enteritis (NE) is responsible for substantial economic losses worldwide annually. Recently, as a result of antibiotic growth promoter prohibition, the prevalence of NE in chickens has reemerged. This study was aimed to reduce NE through titrating dietary deoxycholic acid (DCA) as an effective antimicrobial alternative. Materials and methods:Day-old broiler chicks were assigned to six groups and fed diets supplemented with 0 (basal diet), 0.8, 1.0 and 1.5?g/kg (on top of basal diet) DCA. The birds were challenged with Eimeria maxima (20,000 oocysts/bird) at d 18 and C. perfringens (109?CFU/bird per day) at d 23, 24, and 25 to induce NE. The birds were sacrificed at d 26 when ileal tissue and digesta were collected for analyzing histopathology, mRNA accumulation and C. perfringens colonization by real-time PCR, targeted metabolomics of bile acids, fluorescence in situ hybridization (FISH), or terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) assay. Results:At the cellular level, birds infected with E. maxima and C. perfringens developed subclinical NE and showed shortening villi, crypt hyperplasia and immune cell infiltration in ileum. Dietary DCA alleviated the NE-induced ileal inflammation in a dose-dependent manner compared to NE control birds. Consistent with the increased histopathological scores, subclinical NE birds suffered body weight gain reduction compared to the uninfected birds, an effect attenuated with increased doses of dietary DCA. At the molecular level, the highest dose of DCA at 1.5?g/kg reduced C. perfringens luminal colonization compared to NE birds using PCR and FISH. Furthermore, the dietary DCA reduced subclinical NE-induced intestinal inflammatory gene expression and cell apoptosis using PCR and TUNEL assays. Upon further examining ileal bile acid pool through targeted metabolomics, subclinical NE reduced the total bile acid level in ileal digesta compared to uninfected birds. Notably, dietary DCA increased total bile acid and DCA levels in a dose-dependent manner compared to NE birds. Conclusion:These results indicate that DCA attenuates NE-induced intestinal inflammation and bile acid reduction and could be an effective antimicrobial alternative against the intestinal disease.

Project description:Clostridium perfringens causes enteric diseases in animals and humans. In poultry, avian-specific C. perfringens strains cause necrotic enteritis, an economically significant poultry disease that costs the global industry over $2 billion annually in losses and control measures. With removal of antibiotic growth promoters in some countries this disease appears to be on the rise. In experimental conditions used to study disease pathogenesis and potential control measures, reproduction of the disease relies on the use of predisposing factors such as Eimeria infection and the use of high protein diets, indicating complex mechanisms involved in the onset of necrotic enteritis. The mechanisms by which the predisposing factors contribute to disease progression are not well understood but it has been suggested that they may cause perturbations in the microbiota within the gastrointestinal tract. We inspected changes in cecal microbiota and short chain fatty acids (SCFA) induced by Eimeria and fishmeal, in birds challenged or not challenged with C. perfringens. C. perfringens challenge in the absence of predisposing factors did not cause significant changes in either the alpha or beta diversity of the microbiota nor in concentrations of SCFA. Moreover, there was no C. perfringens detected in the cecal microbiota 2 days post-challenge without the presence of predisposing factors. In contrast, both fishmeal and Eimeria caused significant changes in microbiota, seen in both alpha and beta diversity and also enabled C. perfringens to establish itself post challenge. Eimeria had its strongest influence on intestinal microbiota and SCFA when combined with fishmeal. Out of 6 SCFAs measured, including butyric acid, none were significantly influenced by C. perfringens, but their levels were strongly modified following the use of both predisposing factors. There was little overlap in the changes caused following Eimeria and fishmeal treatments, possibly indicating multiple routes for progressing towards clinical symptoms of necrotic enteritis.

Dataset Information

Bacillus licheniformis normalize the ileum microbiota of chickens infected with necrotic enteritis.

Publications

Bacillus licheniformis normalize the ileum microbiota of chickens infected with necrotic enteritis.

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