Necrotic enteritis in drug-free era
Ontology highlight
ABSTRACT:
PROVIDER: PRJEB40993 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| ERR4770740_1.fastq.gz | Fastqsanger.gz | |||
| ERR4770740_2.fastq.gz | Fastqsanger.gz | |||
| ERR4770750_1.fastq.gz | Fastqsanger.gz | |||
| ERR4770750_2.fastq.gz | Fastqsanger.gz | |||
| ERR4770760_1.fastq.gz | Fastqsanger.gz |
Items per page: 5 1 - 5 of 160 |
Similar Datasets
Project description:This study utilized comparative global gene expression microarray analysis to evaluate the effects of NE on intestinal immunity of chicken. Two-condition experiment, NE-afflicted chickens vs. Non-infected control chickens. Biological replicates: 2 control replicates, 2 NE-afflicted replicates with dye-switching.
2013-09-26 | E-GEOD-51154 | biostudies-arrayexpress
Project description:This study utilized comparative global gene expression microarray analysis to evaluate the effects of NE on intestinal immunity of chicken.
2013-09-26 | GSE51154 | GEO
Project description:Necrotic enteritis (NE), mainly induced by the pathogens of Clostridium perfringens and coccidia, causes huge economic losses with limited intervention options in the poultry industry. This study investigated the role of specific bile acids on NE development. Day-old broiler chicks were assigned to six groups: noninfected, NE, and NE with four bile diets of 0.32% chicken bile, 0.15% commercial ox bile, 0.15% lithocholic acid (LCA), or 0.15% deoxycholic acid (DCA). The birds were infected with Eimeria maxima at day 18 and C. perfringens at day 23 and 24. The infected birds developed clinical NE signs. The NE birds suffered severe ileitis with villus blunting, crypt hyperplasia, epithelial line disintegration, and massive immune cell infiltration, while DCA and LCA prevented the ileitis histopathology. NE induced severe body weight gain (BWG) loss, while only DCA prevented NE-induced BWG loss. Notably, DCA reduced the NE-induced inflammatory response and the colonization and invasion of C. perfringens compared to NE birds. Consistently, NE reduced the total bile acids in the ileal digesta, while dietary DCA and commercial bile restored it. Together, this study showed that DCA and LCA reduced NE histopathology, suggesting that secondary bile acids, but not total bile acid levels, play an essential role in controlling the enteritis.
| S-EPMC8427939 | biostudies-literature
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.
| S-EPMC5701917 | biostudies-literature
Project description:Purpose: Identify at the transcriptome level genes that could be involved in the mode of action of avilamycin, an AGP, when administered at non-therapeutic concentrations, and use this information in regard to development of alternatives to AGPs. Methods: Out of 120 broiler chickens fed either CONTROL feed or AGP feed (supplemented with avilamycin; Surmax® 100, 10 g/1000 kg of feed, Elanco), the RNA from the ileum tissue of five birds per group was isolated from day 35, profiled by RNA-sequencing, and results were verified via RT-qPCR. Results: Overall, 66 differentially expressed genes (DEGs; FDR ≤ 0.05 and fold change ≥ 2 or ≤ -2) were found in the ileum of chicken fed avilamycin in comparison to the control group. Only partial agreement was found on the DEGs (64%) when the reads were initially mapped to the former genome assembly Galgal5 instead of GRCg6a. Functional enrichment analysis showed that the down-regulated DEGs were associated with signaling by interleukins, and that IL-22 and certain antimicrobial peptides could play a central role in the intestinal host response to avilamycin at day 35. This was further corroborated on sixteen chickens per group via RT-qPCR. In addition, higher activity was detected in module of genes related to lipid metabolism and transport in the avilamycin group, as revealed by the co-expression network analysis. Conclusions: Improved feed efficiency was correlated with reduced immunological stress in the intestinal mucosa. The RNA-Seq approach allowed generating novel knowledge that could contribute to the development of AGP alternatives, with IL-22 identified as a potential marker.
2020-12-31 | GSE135272 | GEO
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.
| S-EPMC8501549 | biostudies-literature
Project description:A novel toxin, NetB, has recently been identified in virulent avian Clostridium perfringens isolates and shown to be an essential virulence factor in a clinical necrotic enteritis isolate. To assess whether NetB is more generally associated with avian necrotic enteritis isolates we have screened a range of C. perfringens strains from geographically diverse locations for both the presence and expression of the netB gene. Forty-four isolates were derived from necrotic enteritis disease cases from Australia, Belgium, Denmark and Canada and 55 isolates from healthy chickens from Australia and Belgium. The majority of strains isolated from necrotic enteritis-affected birds were netB positive (70%) and there was an absolute correlation between the presence of netB and in vitro expression of the NetB protein. Only two of the C. perfringens isolates from healthy chickens carried netB. Sequencing of the netB gene from 23 positive isolates showed that NetB is highly conserved, with only one predicted amino acid (A168T) difference, in six isolates, compared to the published sequence. This change did not alter the in vitro activity of the NetB toxin. The gene encoding the recently discovered TpeL toxin was also screened using PCR and only found in a small proportion of NetB-positive isolates from diseased birds. A selection of NetB-negative isolates, originating from diseased birds, was unable to cause disease in a necrotic enteritis induction model. This study provides further evidence that NetB is important in pathogenesis and advances our current understanding of C. perfringens virulence factors in avian necrotic enteritis.
| S-EPMC2797654 | biostudies-literature