Effects of dietary ß-mannanase supplementation on the additivity of true metabolizable energy values for broiler diets.

OBJECTIVE: This experiment was conducted to determine the effects of dietary ß-mannanase on the additivity of true metabolizable energy (TME) and nitrogen-corrected true metabolizable energy (TMEn) for broiler diets. METHODS: A total of 144 21-day-old broilers were randomly allotted to 12 dietary treatments with 6 replicates. Five treatments consisted of 5 ingredients of corn, wheat, soybean meal, corn distillers dried grains with solubles, or corn gluten meal. One mixed diet containing 200 g/kg of those 5 ingredients also was prepared. Additional 6 treatments were prepared by mixing 0.5 g/kg dietary ß-mannanase with those 5 ingredients and the mixed diet. Based on a precision-fed chicken assay, TME and TMEn values for 5 ingredients and the mixed diet as affected by dietary ß-mannanase were determined. RESULTS: Results indicated that when ß-mannanase was not added to the diet, measured TME and TMEn values for the diet did not differ from the predicted values for the diet, which validated the additivity. However, for the diet containing ß-mannanase, measured TMEn value was greater (p<0.05) than predicted TMEn value, indicating that the additivity was not validated. CONCLUSION: In conclusion, the additivity of energy values for the mixed diet may not be guaranteed if the diet contains ß-mannanase.

Graded levels of Eimeria infection modulated gut physiology and temporarily ceased the egg production of laying hens at peak production.

An experiment was conducted to investigate the changes in gastrointestinal physiology, including intestinal leakage, immune response, oxidative stress, along with performance traits, of Hy-Line W-36 laying hens following Eimeria infection at peak egg production. A total of 360 laying hens, at 25 wk of age, were assigned randomly to 5 treatment groups, each consisting of 6 replicate cages, including a nonchallenged control group. The other 4 groups were inoculated with graded levels of mixed Eimeria species as high, medium-high, medium-low, and low doses, respectively. The body weight (BW) and body weight gain (BWG) of laying hens were measured from 0 to 14 days postinoculation (DPI). Average daily feed intake (ADFI) and hen-day egg production (HDEP) were measured from 0 to 15 and 0 to 28 DPI, respectively. Gut permeability was measured on 5 DPI, whereas oxidative stress, immune response, and expression of nutrient transporter genes were measured on 6 and 14 DPI. A significant linear reduction in BW and BWG was observed with increased Eimeria inoculation dosage on both 6 and 14 DPI (P < 0.001, P-Lin < 0.0001). An interaction between the Eimeria dosages and DPI was observed for ADFI (P < 0.0001). Feed intake in the challenged groups decreased starting at 4 DPI, with the most significant drop occurring at 7 DPI, which did not recover until 15 DPI. Following the challenge, gastrointestinal physiology shifted toward the host defense against the Eimeria infection by upregulating mRNA expression of tight junction proteins and immune responses while downregulating the expression of key nutrient transporters on 6 and 14 DPI (P < 0.05). An interaction between the Eimeria inoculation dosage and DPI was also observed for daily HDEP (P < 0.0001). Overall, HDEP was lower in the challenged groups compared to the control. Daily HDEP in the challenged groups dropped from 8 DPI and became similar to the control birds only after 24 DPI. Egg production temporarily ceased in most of the laying hens infected with the high and medium-high dosages of Eimeria. In conclusion, Eimeria infection activated the host immune response, negatively affecting the gastrointestinal health, growth performance, and temporarily ceased the egg production of Hy-Line W-36 laying hens when infected at peak production.

Effect of dietary inclusion of 25-hydroxyvitamin D3 and vitamin E on performance, gut health, oxidative status, and immune response in laying hens infected with coccidiosis.

Vitamin D3 (25-hydroxyvitamin D3 (VD)) and vitamin E (VE) have proven to have immunomodulatory and antioxidant functions along with capacities to improve the reproductive function in chickens. Coccidiosis in laying hens at different stages of growth has been shown to negatively affect performance, immune response, and oxidative status, thus increasing the cost of production. A study was conducted to evaluate the influence of dietary VD or VE on performance, gut health, immune response, and oxidative status of laying hens at peak production. Laying hens (23 wk-of-age, n = 225) were randomly allocated into 5 treatment groups (n = 9 hens/replicate) with 5 replicate groups each: 1) unchallenged control (UC), 2) pair-fed control (PF), 3) challenged control (CC), 4) challenged control top-dressed with 5,000 IU of 25-hydroxyvitamin D3 (VD) per kg of diet, and 5) challenged control top-dressed with 100 IU of DL-α-tocopherol (VE). At 25 wk-of-age, hens grouped in CC, VD, and VE were challenged with mixed Eimeria spp. to induce coccidiosis. VD or VE supplemented hens did not impact bird body weight; however, egg production increased by 10.36% and 13.77%, respectively (P < 0.0001). Furthermore, the gut health of the hens was improved with either VD or VE supplementation, as indicated by lowered gut permeability and intestinal lesion scores (P < 0.05). VE significantly reduced the heterophil count (P = 0.0490) alongside numerically increasing the peripheral CD4+ and CD8+ T cells and monocyte counts (P > 0.05). Both VD or VE increased the TAC at 14 DPI compared to UC (P<0.05). Preliminary findings suggest that dietary VD or VE supplementation has the potential to improve gut health, modulate the immune response, and increase egg production in coccidiosis-infected laying hens.

Comparison of necrotic enteritis effects on growth performance and intestinal health in two different meat-type chicken strains Athens Canadian Random Bred and Cobb 500.

Chickens have undergone genetic improvements in the past few decades to maximize growth efficiency. However, necrotic enteritis (NE), an enteric disease primarily caused by C. perfringens, remains a significant problem in poultry production. A study investigated the differences in intestinal health between the nonselected meat-type chicken Athens Canadian Random Bred (ACRB) and the modern meat-type Cobb 500 broilers (Cobb) when challenged with experimental NE. The study utilized a 2 × 3 factorial arrangement, consisting of two main effects of chicken strain and NE challenge model (nonchallenged control, NC; NE challenge with 2,500/12,500 Eimeria maxima oocysts + 1 × 109C. perfringens, NE2.5/NE12.5). A total of 432 fourteen-day-old male ACRB and Cobb were used until 22 d (8 d postinoculation with E. maxima on d 14, dpi), and the chickens were euthanized on 6 and 8 dpi for the analysis. All data were statistically analyzed using a two-way ANOVA, and Student's t-test or Tukey's HSD test was applied when P < 0.05. The NE12.5 group showed significant decreases in growth performance and relative growth performance from d 14 to 20, regardless of chicken strain (P < 0.01). The ACRB group exhibited significant decreases in relative body weight and relative body weight gain compared to the Cobb group from d 14 to 22 (P < 0.01). On 6 and 8 dpi, both NE challenge groups showed significant decreases in intestinal villus height to crypt depth ratio, jejunal goblet cell count, and jejunal MUC2 and LEAP2 expression (P < 0.01). Additionally, the NE12.5 group had significantly higher intestinal NE lesion score, intestinal permeability, fecal E. maxima oocyst count, intestinal C. perfringens count, and jejunal IFNγ and CCL4 expression compared to the NC group (P < 0.05). In conclusion, NE negatively impacts growth performance and intestinal health in broilers, parameters regardless of the strain.

Different dietary branched-chain amino acid ratios, crude protein levels, and protein sources can affect the growth performance and meat yield in broilers.

Balanced ratios of branched-chain amino acids (BCAAs) can enhance chicken growth, immunity, and muscle synthesis. However, these ratios can be affected by changes in crude protein (CP) levels or the substitution of protein sources, leading to BCAA antagonism. This, in turn, can have a negative impact on chicken growth. In Experiment 1, a total of 960 0-d-old male Cobb 500 broilers were divided into 6 treatments with 8 replicates. Three different BCAA ratios were used in High or Low CP diets as follows: 1) Low Leu group (Low level of leucine with increased valine and isoleucine levels), 2) Med Leu group, and 3) High Leu group (High level of leucine with reduced valine and isoleucine levels) for a total of 6 diets. In Experiment 2, a total of 640 0-d-old male Cobb 500 broilers were divided into 4 treatments with 8 replicates. The four diets had either High or Low CP and one of two protein sources with the same medium levels of BCAAs: 1) the soybean meal (SBM) group, which had SBM as the main protein source (protein bound AA), and 2) the wheat middlings with non-bound AAs (WM+AA) group (non-bound AA), which had additional non-bound AAs to replace SBM. The High Leu diet had a negative effect on overall growth performance, carcass weight, breast muscle weight, and body mineral composition compared to the Low Leu and Med Leu groups, particularly in the High CP diet (P < 0.05). The SBM group showed increased growth performance, breast muscle weight, expression levels of genes promoting muscle growth, and improved bone mineral composition compared to the WM+AA group, and the High CP group intensified the negative effect of the WM+AA diet (P < 0.05). In summary, balanced BCAA ratios and SBM-based diets have positive effects on chicken growth and muscle accretion, whereas excessive leucine and non-bound AA levels in the diets may negatively affect growth performance and meat yield in chickens.

Characterization of Collagen Binding Activity of Clostridium perfringens Strains Isolated from Broiler Chickens.

Clostridium perfringens is the etiological agent for necrotic enteritis (NE) in broiler chickens, which causes a substantial economic loss of an estimated USD 6 billion annually in the global poultry industry. Collagen adhesion is involved in the NE pathogenesis in poultry. In this study, the binding capabilities of chicken C. perfringens isolates of various genetic backgrounds (netB-tpeL-, netB+tpeL-, netB+tpeL+) to collagen types I-V and gelatin were examined, and the putative adhesin protein cnaA gene was investigated at the genomic level. In total, 28 C. perfringens strains from healthy and NE-inflicted sick chickens were examined. The results on collagen adhesin-encoding gene cnaA by the quantitative-PCR results indicated that netB-tpeL- isolates had much lower copies of the detectable cnaA gene than netB+ isolates (10 netB+tpeL- isolates, 5 netB+tpeL+ isolates). Most of the virulent C. perfringens isolates demonstrated collagen-binding abilities to types I-II and IV-V, while some strains showed weak or no binding to collagen type III and gelatin. However, the netB+tpeL+ isolates showed significantly higher binding capabilities to collagen III than netB-tpeL- and netB+tpeL- isolates. The data in this study suggest that the collagen-binding capability of clinical C. perfringens isolates correlates well with their NE pathogenicity levels, especially for C. perfringens isolates carrying genes encoding crucial virulence factors and virulence-associated factors such as netB, cnaA, and tpeL. These results indicate that the presence of the cnaA gene may be correlated with C. perfringens virulence (particularly for netB+ isolates).

Effects of Different Eimeria Inoculation Doses on Growth Performance, Daily Feed Intake, Gut Health, Gut Microbiota, Foot Pad Dermatitis, and Eimeria Gene Expression in Broilers Raised in Floor Pens for 35 Days.

The study was conducted to investigate the effects of different Eimeria inoculation doses on the growth performance, gut ecosystem, and body composition of broilers in floor pens for 35 days. A total of 750 15-day-old broilers were allocated to five experimental groups with six replicate pens. The five experimental groups included unchallenged control (CON); Eimeria dose 1 (ED1): E. acervulina: 31,250/E. maxima: 6250/E. tenella: 6250; Eimeria dose 2 (ED2): E. acervulina: 62,500/E. maxima: 12,500/E. tenella: 12,500; Eimeria dose 3 (ED3): E. acervulina: 125,000/E. maxima: 25,000/E. tenella: 25,000; and Eimeria dose 4 (ED4): E. acervulina: 250,000/E. maxima: 50,000/E. tenella: 50,000. On D 21, BW were linearly reduced by increased Eimeria inoculation doses (p < 0.01). On D 35, the Eimeria challenge groups had significantly lower BW compared to the CON group. Increased Eimeria inoculation doses linearly decreased crude fat (CF) (p < 0.01) on D 21. Increased Eimeria inoculation doses tended to increase the relative abundance of the phylum Proteobacteria (p = 0.098) on D 21. On D 35, lean:fat was linearly reduced by increased Eimeria inoculation doses (p < 0.05). Eimeria infection negatively influenced growth performance and gut health in broilers in the acute phase, and the negative effects were prolonged to D 35 in floor pen conditions.

Effects of Eimeria maxima infection doses on growth performance and gut health in dual-infection model of necrotic enteritis in broiler chickens.

The objective of this study was to investigate the effects of the different doses of Eimeria maxima (EM) oocysts on growth performance and intestinal health in broiler chickens challenged with a dual infection model of necrotic enteritis (NE) using EM and NetB+ Clostridium perfringens (CP). A total of 432 fourteen-d-old male Cobb 500 broiler chickens were divided into 6 groups with 6 replicates each. The six different groups were as follows: Control, non-challenged; T0+, challenged with CP at 1 × 109 colony forming unit; T5K+, T0+ + 5,000 EM oocysts; T10K+, T0+ + 10,000 EM oocysts; T20K+; T0+ + 20,000 EM oocysts; and T40K+; T0+ + 40,000 EM oocysts. The challenge groups were orally inoculated with EM strain 41A on d 14, followed by NetB+ CP strain Del-1 on 4 days post inoculation (dpi). Increasing EM oocysts decreased d 21 body weight, body weight gain, feed intake (linear and quadratic, p < 0.001), and feed efficiency (linear, p < 0.001) from 0 to 7 dpi. Increasing EM oocysts increased jejunal NE lesion score and intestinal permeability on 5, 6, and 7 dpi (linear, p < 0.05). On 7 dpi, increasing the infection doses of EM oocysts increased jejunal CP colony counts (linear, p < 0.05) and increased fecal EM oocyst output (linear and quadratic, p < 0.001). Furthermore, increasing the infection doses of EM oocysts decreased the villus height to crypt depth ratios and the goblet cell counts (linear, p < 0.05) on 6 dpi. Increasing EM oocysts downregulated the expression of MUC2, B0AT, B0,+AT, PepT1, GLUT2, AvBD3 and 9, LEAP2, and TLR4, while upregulating CLDN1, CATHL3, IL-1ß, IFN-γ, TNFSF15, TNF-α, IL-10, and Gam56 and 82 on 6 dpi (linear, p < 0.05). Additionally, increasing EM oocysts decreased Pielou's evenness and Shannon's entropy (linear, p < 0.01). In conclusion, increasing the infection doses of EM significantly aggravated the severity of NE and exerted negative impact on intestinal health from 5 to 7 dpi.

Effect of dietary sophorolipids on growth performance and gastrointestinal functionality of broiler chickens infected with Eimeria maxima.

Two experiments were conducted to evaluate the effects of dietary sophorolipids (SLs) supplementation as antibiotic alternatives on growth performance and gut health of chickens infected with Eimeria maxima. In experiment 1, 336 (zero-day-old) male broilers were used. The chickens were weighed and randomly allocated to the following 6 treatments groups with 7 chickens/cage and 8 cages/treatment: control group that received a basal diet (NC), positive control group that received a basal diet and was challenged with E. maxima (PC), PC+C18:1 lactonic diacetyled SL (SL1), PC+C18:1 deacetyled SL (SL2), PC+C18:1 monoacetyled SL (SL3), and PC+C18:1 diacetyled SL (SL4). Each SL (200 mg/kg feed) was added to the corresponding treatment group. In experiment 2, 588 (zero-day-old) male broilers were used. The chickens were randomly allocated to the following experimental groups with 10 or 11 chickens/cage and 8 cages/treatment: NC, PC, PC+ monensin at 90 mg/kg feed (MO), PC+SL1 at 200 mg/kg feed (SL1 200), PC+SL1 at 500 mg/kg feed (SL1 500), PC+SL4 at 200 mg/kg feed (SL4 200), and PC+SL4 at 500 mg/kg of feed (SL4 500). The chickens and feed were weighed at 0, 7, 14, 20, and 22 d to determine growth performance. In both experiments, all chickens except the NC group were orally infected with E. maxima (10,000 oocysts/chicken) at d 14. One chicken per cage was euthanized at d 20 to sample jejunal tissue to measure lesion scores, cytokines, and tight junction (TJ) proteins. Excreta samples were collected daily between d 20 and 22 to measure oocyst numbers. Data were analyzed using Mixed Model (PROC MIXED) in SAS. In experiment 1, SLs did not affect the growth of broiler chickens, but SL4 decreased (P < 0.05) the lesion score and oocyst number compared to PC chickens. In terms of cytokines and TJ protein gene expression, SLs increased (P < 0.05) IL-1ß, IL-6, IL-17F, IL-4, IL-13, occludin, and ZO1 levels compared to PC chickens. In experiment 2, monensin increased (P < 0.05) body weight, and decreased (P < 0.05) the lesion score and oocyst number compared to the PC group. SL4 500 increased (P < 0.05) average daily gain and feed conversion ratio but decreased (P < 0.05) lesion score and fecal oocyst number. SL4 decreased (P < 0.05) IL-6, IL-17F, TNFSF-15, IL-2, and IL-10 levels but increased (P < 0.05) occludin and ZO-1 levels. Overall, dietary SL supplementation, especially SL4, improved growth and gastrointestinal functionality of young broiler chickens, demonstrating significant potential as an antibiotic alternative.

Effects of tannic acid supplementation on growth performance, gut health, and meat production and quality of broiler chickens raised in floor pens for 42 days.

A study was conducted to investigate the effects of tannic acid (TA) supplementation on growth performance, gut health, antioxidant capacity, gut microbiota, and meat yield and quality in broilers raised for 42 days. A total of 700 one-day-old male broiler chickens (Cobb500) were allocated into 5 treatments with 7 replicates of 20 birds per pen. There were five treatments: 1) tannic acid 0 (TA0: basal diet without TA); 2) tannic acid 0.25 (TA0.25: basal diet+0.25 g/kg TA); 3) tannic acid 0.5 (TA0.5: basal diet+0.5 g/kg TA); 4) tannic acid 1 (TA1: basal diet+1 g/kg TA); and 5) tannic acid 2 (TA2: basal diet+2 g/kg TA). The dietary phases included starter (D 0 to 18; crumble feed), grower (D 18 to 28; pellet feed), and finisher (D 28 to 42; pellet feed). On D 18, the supplementation of TA linearly reduced body weight (BW) and average daily feed intake (ADFI) (p < 0.05), and on D 28, the supplementation of TA linearly reduced BW, average daily gain (ADG), and feed conversion ratio (FCR) (p < 0.05). Relative mRNA expression of genes related to mucin production (MUC2), tight junction proteins (CLDN2 and JAM2), and nutrient transporters (B0AT1 and SGLT1) was linearly increased by the supplementation of TA (p < 0.05). The supplementation of TA tended to linearly increase the relative abundance of the family Enterobacteriaceae (p = 0.08) and quadratically increased the relative abundance of the families Lachnospiraceae and Ruminococcaceae in the cecal microbial communities (p < 0.05). On D 36, the ratio of the phyla Firmicutes and Bacteroidetes was quadratically reduced by the supplementation of TA (p < 0.05). On D 42, bone mineral density and the lean to fat ratio were linearly decreased by the supplementation of TA (p < 0.05). On D 43, total chilled carcass weight was linearly reduced (p < 0.05), and proportion of leg weight was increased by supplementation of TA (p < 0.05). The supplementation of TA linearly reduced pH of the breast meat (p < 0.05) and linearly increased redness (a*) (p < 0.05). Although the supplementation of TA positively influenced gut health and gut microbiota in the starter/grower phases, it negatively affected overall growth performance, bone health, and meat production in broilers on D 42.

Gut Microbiota-Derived Indole-3-Carboxylate Influences Mucosal Integrity and Immunity Through the Activation of the Aryl Hydrocarbon Receptors and Nutrient Transporters in Broiler Chickens Challenged With Eimeria maxima.

Two studies were conducted to evaluate the effects of indole-3-carboxylate (ICOOH) as a postbiotic on maintaining intestinal homeostasis against avian coccidiosis. In the first study, an in vitro culture system was used to investigate the effects of ICOOH on the proinflammatory cytokine response of chicken macrophage cells (CMCs), gut integrity of chicken intestinal epithelial cells (IECs), differentiation of quail muscle cells (QMCs), and primary chicken embryonic muscle cells (PMCs) and anti-parasitic effect against Eimeria maxima. Cells to be tested were seeded in the 24-well plates and treated with ICOOH at concentrations of 0.1, 1.0, and 10.0 µg. CMCs were first stimulated by lipopolysaccharide (LPS) to induce an innate immune response, and QMCs and PMCs were treated with 0.5% and 2% fetal bovine serum, respectively, before they were treated with ICOOH. After 18 h of incubation, cells were harvested, and RT-PCR was performed to measure gene expression of proinflammatory cytokines of CMCs, tight junction (TJ) proteins of IECs, and muscle cell growth markers of QMCs and PMCs. In the second study, in vivo trials were carried out to study the effect of dietary ICOOH on disease parameters in broiler chickens infected with E. maxima. One hundred twenty male broiler chickens (0-day-old) were allocated into the following four treatment groups: 1) basal diet without infection (CON), 2) basal diet with E. maxima (NC), 3) ICOOH at 10.0 mg/kg feed with E. maxima (HI), and 4) ICOOH at 1.0 mg/kg feed with E. maxima (LO). Body weights (BWs) were measured on 0, 7, 14, 20, and 22 days. All groups except the CON chickens were orally infected with E. maxima on day 14. Jejunal samples were collected for lesion score and the transcriptomic analysis of cytokines and TJ proteins. In vitro, ICOOH increased the expression of TJ proteins in IECs and decreased IL-1ß and IL-8 transcripts in the LPS-stimulated CMCs. In vivo, chickens on the HI diet showed reduced jejunal IL-1ß, IFN-γ, and IL-10 expression and increased expression of genes activated by aryl hydrocarbon receptors and nutrient transporters in E. maxima-infected chickens. In conclusion, these results demonstrate the beneficial effects of dietary ICOOH on intestinal immune responses and barrier integrity in broiler chickens challenged with E. maxima. Furthermore, the present finding supports the notion to use microbial metabolites as novel feed additives to enhance resilience in animal agriculture.

Effects of Dietary Maltol on Innate Immunity, Gut Health, and Growth Performance of Broiler Chickens Challenged With Eimeria maxima.

Two studies were conducted to evaluate the effects of maltol as a postbiotic on innate immunity, gut health, and enteric infection. In the first study, an in vitro culture system was used to evaluate the effects of maltol on the innate immune response of chicken macrophage cells (CMC), gut integrity of chicken intestinal epithelial cells (IEC), anti-parasitic activity against Eimeria maxima, and differentiation of quail muscle cells (QMC) and primary chicken embryonic muscle cells (PMC). All cells seeded in the 24-well plates were treated with maltol at concentrations of 0.1, 1.0, and 10.0 µg. CMC and IEC were stimulated by lipopolysaccharide to induce an innate immune response, and QMC and PMC were treated with 0.5 and 2% fetal bovine serum, respectively. After 18 h of incubation, pro-inflammatory cytokines, tight junction proteins (TJPs), and muscle cell growth markers were measured. In the second study, the dietary effect of maltol was evaluated on disease parameters in broiler chickens infected with E. maxima. Eighty male 1-day-old broiler chickens were allocated into the following four treatment groups: (1) Control group without infection, (2) Basal diet with E. maxima, (3) High maltol (HI; 10.0 mg /kg feed) with E. maxima, and (4) Low maltol (LO; 1.0 mg/kg feed) with E. maxima. Body weights (BW) were measured on days 0, 7, 14, 20, and 22. All chickens except the CON group were orally infected with 104 E. maxima per chicken on day 14. Jejunum samples were collected for gut lesion scoring, and the gene expression of cytokines and TJPs. Data was analyzed using PROC MIXED in SAS. In vitro, maltol not only increased TJPs in IEC and cytokines in the LPS-stimulated CMC but also showed direct cytotoxicity against sporozoites of E. maxima. In vivo, the HI group improved the BW, reduced the gut lesion scores and fecal oocyst shedding, and decreased jejunal TNFSF15 and IL-1ß expression in E. maxima-infected chickens. In conclusion, these results demonstrate the beneficial effects of dietary maltol in the enhancement of growth performance, gut health, and coccidiosis resistance and the applicability of maltol as a postbiotic for the replacement of antibiotic growth promoters in commercial poultry production.

The effects of dietary Bacillus subtilis supplementation, as an alternative to antibiotics, on growth performance, intestinal immunity, and epithelial barrier integrity in broiler chickens infected with Eimeria maxima.

The objective of this study was to investigate the effects of dietary Bacillus subtilis supplementation on growth performance, jejunal lesion scores, oocyst shedding, and cytokine and tight junction protein expression in broiler chickens infected with Eimeria maxima. A total of 196 male day-old Ross 708 broilers were given a nonexperimental diet until 14 D of age. Then, all chickens were randomly assigned to one of seven dietary treatments: 2 basal diets (CON and NC); CON + virginiamycin (AB1); CON + bacitracin methylene disalicylate (BMD; AB2); CON + B. subtilis 1781 (PB1); CON + B. subtilis 747 (PB2); or CON + B. subtilis 1781 + 747 (PB3). At day 21, all chickens except those in the CON group were orally inoculated with E. maxima oocysts. At 7 D after E. maxima infection, the body weight gains of chickens fed PB2 and PB3 increased (P = 0.032) as much as those in chickens fed AB2. The body weight gain and feed efficiency of chickens fed PB2 were significantly increased (P < 0.001), and PB2 chickens showed (P = 0.005) the lowest lesion scores after E. maxima infection. Chickens fed PB2 showed (P < 0.05) lower mRNA expression of IL-1ß in infected chicken groups. Chickens in the AB1, AB2, PB1, PB2, and PB3 groups showed (P < 0.05) greater mRNA expression of junctional adhesion molecule 2 in jejunal tissue, whereas occludin expression increased (P < 0.05) in the jejunal tissue of chickens fed AB2 or PB2. Dietary B. subtilis supplementation significantly improved the growth performance of young chickens to a level comparable with that induced by virginiamycin or BMD without E. maxima infection. After infection with E. maxima, dietary virginiamycin and BMD significantly enhanced the epithelial barrier integrity, and the dietary B. subtilis 747 showed significantly enhanced growth performance, intestinal immunity, and epithelial barrier integrity. Together our results indicated that certain strains of B. subtilis provide beneficial effects on the growth of young broiler chickens and have the potential to replace antibiotic growth promoters.

Effect of Heat Stress and Stocking Density onGrowth Performance, Breast Meat Quality,and Intestinal Barrier Function in Broiler Chickens.

The present experiment was conducted to investigate the effect of heat stress (HS) andstocking density (SD) on growth performance, breast meat quality, and intestinal barrier functionin broiler chickens. Experimental treatments included two different ambient temperatures (20 °C:thermoneutral conditions, or 27.8 °C: HS conditions) and two different SD (low: 9 birds/m2 andhigh: 18 birds/m2) in a 2 × 2 factorial arrangement. A total of 1140 21-day-old broiler chickens wereallotted 1 of 4 treatments with five replicates. At the end of the experiment (35 days of age), twobirds per replicate were euthanized for sample collections. The results indicated no interactionsbetween HS and SD for all measurements. For main effects, HS decreased (p < 0.05) the growthperformance of broiler chickens. Similarly, high SD also decreased (p < 0.05) body weight gain andfeed intake. HS decreased (p < 0.01) jejunal trans-epithelial electric resistance (TER), whereas highSD did not affect TER. Neither HS nor high SD affected jejunal tight junction-related geneexpressions; however, high SD reduced (p < 0.05) occludin expression. In conclusion, HS and highSD are key environmental factors decreasing broiler performance; however, the interactive effectsof HS and high SD are not significant under the current conditions.