Dataset Information

Interactive effect of dietary calcium and phytase on broilers challenged with subclinical necrotic enteritis: part 2. Gut permeability, phytate ester concentrations, jejunal gene expression, and intestinal morphology.

ABSTRACT: Calcium has the capacity to interact with phytate-P to form Ca-phytate complexes and decrease the ability of exogenous phytase to degrade phytic acid. This study investigated the hypothesis that high dietary Ca would impair gut permeability, phytate esters (inositol x-phosphate, IPx: IP3, IP4, IP5, and IP6) degradation, jejunal gene expression, and intestinal morphology. Ross 308 day-old male broilers (n = 768) were distributed into 48-floor pens each housing 16 birds in a factorial arrangement. Factors were NE challenge-no or yes; phytase level of 500 or 1,500 FTU/kg, and Ca level 0.6 or 1.0% starter, 0.5 or 0.9% grower, 0.4 or 0.8% finisher with available P in each phase. Challenged birds were gavaged with 3 field strains of Eimeria on day 9 and 10⁸ CFU per mL of Clostridium perfringens Strain EHE-NE18 on day 14 and day 15. A phytase × Ca interaction was observed in the ileum for IP3 (P < 0.01), IP4 (P < 0.05), and IP6 (P < 0.01). The IP3 and IP4 concentrations were similar for both doses of phytase in the presence of low Ca, but with high Ca, both increased significantly but to a greater extent when the high dose of phytase was used. While IP6 concentrations were low and similar between both doses of phytase at low Ca levels, increasing dietary Ca levels increased IP6 concentrations regardless of phytase dose, but the effect was greater in the low phytase diet. A phytase × Ca interaction was detected for vitamin D receptor (VDR) (P < 0.05) expression where bird fed low phytase and low Ca recorded the highest expression of VDR, all other treatments being equivalent. The challenge decreased crypt depth to villus height ratio (P < 0.001). Challenge birds had higher fluorescein isothiocyanate dextran (P < 0.05) in blood compared with unchallenged birds. Thus, high Ca and high phytase, while not the best for IP6 destruction, did not lead to huge reductions in indicators of gut health.

SUBMITTER: Zanu HK

PROVIDER: S-EPMC7598120 | biostudies-literature | 2020 Oct

REPOSITORIES: biostudies-literature

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Interactive effect of dietary calcium and phytase on broilers challenged with subclinical necrotic enteritis: part 2. Gut permeability, phytate ester concentrations, jejunal gene expression, and intestinal morphology.

Zanu H K HK Kheravii S K SK Morgan N K NK Bedford M R MR Swick R A RA

Poultry science 20200703 10

Calcium has the capacity to interact with phytate-P to form Ca-phytate complexes and decrease the ability of exogenous phytase to degrade phytic acid. This study investigated the hypothesis that high dietary Ca would impair gut permeability, phytate esters (inositol x-phosphate, IPx: IP3, IP4, IP5, and IP6) degradation, jejunal gene expression, and intestinal morphology. Ross 308 day-old male broilers (n = 768) were distributed into 48-floor pens each housing 16 birds in a factorial arrangement. ...[more]

PMID: 32988528

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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: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:BackgroundBacteriophages are viral predators of bacteria and are common in nature. Their host-specific infections against specific bacteria make them an attractive natural agent to control bacterial pathogens. Interest in the potential of bacteriophages as antibacterial agents in the production animal industries has increased.MethodsA total of 18 bacteriophages were isolated from Australian commercial poultry environments, from which three highly active phages were chosen for enrichment. Sequencing libraries were prepared using a Nextera XT kit (Illumina) and sequenced on an Illumina MiSeq instrument using 2 × 300 bp paired-end chemistry. The sequence data were then assembled and aligned with a2 bacteriophage as the reference. An animal trial was performed by oral gavaging Clostridium perfringens netB containing strain EHE-NE18 to the Ross 308 broiler chickens prior inoculation with Eimeria species. The chickens were raised following the management guide for Ross 308 from d 0 to d 21 and fed with starter and grower diets met the specific breed nutrient requirements. Body weight gain and feed intake were measured on d 9 and d 21 and FCR adjusted with mortality was calculated.ResultsThe isolated bacteriophages only had only 96.7% similarity to the most closely related, previously characterized, Clostridium bacteriophage indicated that they might represent a novel strain of bacteriophage. A "cocktail" containing the three bacteriophages was capable of lysing four known disease-inducing C. perfringens strains in vitro. Oral administration of the bacteriophages cocktail to broilers challenged with necrotic enteritis markedly alleviated intestinal necrotic lesions in the duodenum and jejunum on day 16 post-hatch. The phage treatment significantly reduced the lesion scores of birds challenged with NE (P < 0.01), and the lesion scores between birds treated with the bacteriophages and the unchallenged birds were not statistically different (P > 0.05). However, no effect on the growth performance was observed during the recorded period of days 9-21.ConclusionThese findings suggest that bacteriophage treatment is a promising approach to protect intestinal health from C. perfringens induced necrotic enteritis. Further research will be required on the dosing, route of administration, and large scale validation studies to further advance this approach to pathogen control.

Project description:Necrotic enteritis (NE) is an infection of the gastrointestinal tract and is estimated to cost the global poultry industry billions of dollars annually. A study was conducted to examine whether reducing the crude protein might offset the severity of NE in broilers experimentally challenged with Eimeria spp. on day 9 and Clostridium perfringens on days 14 and 15. Furthermore, increasing the dietary amino acid (AA) density of the diet was also examined owing to identified benefits of improving performance compromised from low protein (LP) diets or NE. A 2 × 2 × 3 factorial arrangement of treatments at 6 replicates per treatment was used with 972 Ross 308 cockerels fed wheat-sorghum-soy-based diets to 35 D. Factors were NE challenge: no or yes; protein: standard (SP) or LP; and AA density: 100% AA, 115% with only essential AA (115% EAA) increased, and 115% AA with both essential and nonessential AA (115% AA) increased. The performance was measured in grower (days 7-21), finisher (days 21-35), and overall (day 7-35) periods. In addition, on day 16, intestinal lesion score and cecal short-chain fatty acids were measured. Only in nonchallenged birds fed LP diets, 115% AA increased grower feed intake (P < 0.01) and body weight gain (P < 0.05) compared to 115% EAA treatments. Challenge increased jejunal lesions (P < 0.001) with no difference between dietary treatments. Finisher body weight gain was greater in nonchallenged birds fed the 115% AA diets than in challenged birds (P < 0.05). Feeding diets with higher nonessential AA encouraged faster recovery from NE challenge. When fed the SP diets, NE challenge increased cecal butyric acid (P < 0.01) and total short-chain fatty acids (P < 0.05). The nutrient matrix used in LP diets does not favor beneficial butyric acid-producing bacteria. Using LP diets to mitigate NE severity does not offset the predisposing effect of E. spp. when attacking the gastrointestinal tract, and NE recovery is favored when feeding SP diets or additional AA.

Project description:BackgroundNecrotic enteritis (NE) is a severe intestinal infection that affects both humans and poultry. It is caused by the bacterium Clostridium perfringens (CP), but the precise mechanisms underlying the disease pathogenesis remain elusive. This study aims to develop an NE broiler chicken model, explore the impact of the microbiome on NE pathogenesis, and study the virulence of CP isolates with different toxin gene combinations.MethodsThis study established an animal disease model for NE in broiler chickens. The methodology encompassed inducing abrupt protein changes and immunosuppression in the first experiment, and in the second, challenging chickens with CP isolates containing various toxin genes. NE was evaluated through gross and histopathological scoring of the jejunum. Subsequently, jejunal contents were collected from these birds for microbiome analysis via 16S rRNA amplicon sequencing, followed by sequence analysis to investigate microbial diversity and abundance, employing different bioinformatic approaches.ResultsOur findings reveal that CP infection, combined with an abrupt increase in dietary protein concentration and/or infection with the immunosuppressive variant infectious bursal disease virus (vIBDV), predisposed birds to NE development. We observed a significant decrease (p < 0.0001) in the abundance of Lactobacillus and Romboutsia genera in the jejunum, accompanied by a notable increase (p < 0.0001) in Clostridium and Escherichia. Jejunal microbial dysbiosis and severe NE lesions were particularly evident in birds infected with CP isolates containing cpa, netB, tpeL, and cpb2 toxin genes, compared to CP isolates with other toxin gene combinations. Notably, birds that did not develop clinical or subclinical NE following CP infection exhibited a significantly higher (p < 0.0001) level of Romboutsia. These findings shed light on the complex interplay between CP infection, the gut microbiome, and NE pathogenesis in broiler chickens.ConclusionOur study establishes that dysbiosis within the jejunal microbiome serves as a reliable biomarker for detecting subclinical and clinical NE in broiler chicken models. Additionally, we identify the potential of the genera Romboutsia and Lactobacillus as promising candidates for probiotic development, offering effective alternatives to antibiotics in NE prevention and control.

Project description:The primary cause of necrotic enteritis (NE) disease in chickens is the NetB-positive Clostridium perfringens bacterium. Many factors are known to affect the severity of NE in the challenge models of broiler chickens, and one of these factors is the virulence of C. perfringens strain. This study was conducted to evaluate the effect of 2 pathogenic C. perfringens strains in a NE challenge model on gut health and mRNA expression of genes encoding apoptosis, tight junction, immunity, and nutrient transporters in broilers. Day-old Ross-308 male broilers (n = 468) were allocated in a 2 × 3 factorial arrangement of treatments with in-feed antibiotics (no or yes) and challenge (Non, C. perfringens strain NE18, and C. perfringens strain NE36) as the factors. The birds in the challenged groups were inoculated with Eimeria species on day 9 and with a fresh suspension of C. perfringens NE18 or NE36 on day 14 and 15. Sample collection was performed on 2 birds of each pen on day 16. Necrotic enteritis challenge, impaired feed conversion ratio during day 0 to 16 compared with the control group where the effect of the NE36 challenge was more severe than that with NE18 (P < 0.001). The mRNA expression of mucin-2, immunoglobulin-G, occludin (P < 0.001), and tight junction protein-1 (P < 0.05) genes were downregulated in both challenged groups compared with the nonchallenged counterparts. Antibiotic supplementation, on the other hand, increased weight gain, and feed intake in all challenged birds (P < 0.01), but upregulated mucin-5ac and alanine, serine, cysteine, and threonine transporter-1 (P < 0.05) only in the NE18 challenged birds. The challenge with NE36 significantly upregulated caspase-8 and claudin-1 (P < 0.001), but downregulated glucose transporter-2 (P < 0.001) compared with the NE18 challenge. These results suggest that NE challenge is detrimental to the performance of broilers through compromised intestinal health, and different C. perfringens strains can affect the severity of the disease through modulating the expression of intestinal genes encoding proteins responsible for apoptosis, gut integrity, immunity, mucus production, and nutrient transporters.

Dataset Information

Interactive effect of dietary calcium and phytase on broilers challenged with subclinical necrotic enteritis: part 2. Gut permeability, phytate ester concentrations, jejunal gene expression, and intestinal morphology.

Publications

Interactive effect of dietary calcium and phytase on broilers challenged with subclinical necrotic enteritis: part 2. Gut permeability, phytate ester concentrations, jejunal gene expression, and intestinal morphology.

Similar Datasets

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