This study investigated the effects of dietary lactulose supplementation on broiler growth performance, intestinal histomorphology, cecal microflora, and cecal short-chain fatty acid (SCFA) concentrations. A total of 245 one-day-old male broiler chickens were randomly assigned to 5 different treatments, with 7 replicates including 7 birds each. The birds received the same basal diet based on corn--soybean meal, and lactulose was included in the diet at 0, 0.2, 0.4, 0.6, or 0.8% at the expense of corn and/or soybean meal. The body weight gain (linear, P=0.027) and feed conversion (linear, P=0.003) from 0 to 21 d showed significant improvement as dietary lactulose was increased from 0.2 to 0.8%. However, dietary lactulose did not affect broiler performance at the end of the experiment (42 d). Furthermore, intestinal measurements and the goblet cell count of broilers fed a lactulose-containing diet differed from those of birds fed a diet that did not contain lactulose. In addition, a significant quadratic response in the Lactobacillus count (P≤0.001) was observed at 42 d on increasing the level of lactulose. The cecal coliform bacterial population was not affected by the dietary treatments. Supplementation with lactulose significantly increased the concentrations of acetate, propionate, butyrate, and total SCFA measured on d 7 and d 42. In conclusion, inclusion of lactulose in the diet can enhance broiler performance and intestinal morphology by selectively stimulating intestinal microflora and increasing cecal SCFA concentrations.

Necrotic enteritis (NE) continues to present major challenges to the poultry industry, and the etiologic agent Clostridium perfringens is the fourth leading cause of bacterially-induced food- borne illnesses in the US. This study was designed to evaluate the effects of a probiotic during naturally occurring NE. On day of hatch, 1080 Cobb 500 male broilers were randomly allocated to three groups (12 replicate pens/treatment, 30 birds/pen) including 1) negative control (NC): corn-soybean meal diet; 2) positive control (PC): NC + 20 mg virginiamycin/kg diet (0.450 kg Stafac®20/ton); and 3) NC + PrimaLac (1.36 and 0.91 kg/ton from 1–21 and 22–42 days, respectively). One day (d) post placement, all birds were challenged by a commercial live oocyst coccidia vaccine as a predisposing factor to NE. Body weight and feed intake were measured at the onset of NE (d 8) and end of each feeding phase. On d 8, small intestines of two birds/pen were examined for NE lesions, and jejunum samples from one bird were collected for mRNA gene expression analysis of tight junction proteins, cytokines, and nutrient transporters. Data were analyzed using the Jump (JMP) software and significance between treatments identified by LSD (P < 0.05). Compared to NC, supplementation of probiotic reduced d 1–42 mortality; however, PC was the only group with significantly lower mortality. Despite significantly improved feed conversion ratio (FCR) in PC and probiotic groups during d 1–42, average daily gain was only higher in PC (77.69 g/bird) compared with NC (74.99 g/bird). Furthermore, probiotic and PC groups had significantly reduced lesion scores in the duodenum and jejunum compared to NC. Expression of claudin-3 was higher, while expression of zonula occluden-2 tended (P = 0.06) to be higher in probiotic-supplemented birds compared to NC. Moreover, birds fed the probiotic diet had significantly higher expression of IL-10, IL-17, AMPK-α1, and SGLT1 mRNA compared to NC birds. The expression of PepT1 was higher for the probiotic-supplemented group compared to PC. IFN-γ expression was lower in PC compared to NC, while there was no difference between probiotic and NC. There were no differences in gene expression of sIgA, TNF-α, IL-1β, and IL-22 among treatments. Collectively, these data indicate that in a naturally occurring NE model, supplementation of a probiotic helps to improve FCR and reduce lesions, potentially due to the improvements in mRNA expression of tight junctions, cytokines, and nutrient transporters.

The withdrawal of antibiotic growth promoters from poultry feed has increased the risk of necrotic enteritis (NE) outbreaks. This study examined the effects of a probiotic (PROB) or probiotic/prebiotic/essential oil supplement (PPEO) during a subclinical NE challenge. On day (d) of hatch, 960 male broilers were randomized to four groups (8 pens/treatment, 30 birds/pen) including (1) negative control (NC): corn-soybean meal diet; (2) positive control (PC): NC + 20 g Virginiamycin/ton diet; (3) NC + 227 g PROB/ton diet; and (4) NC + 453 g PPEO/ton diet. One d after placement, birds were challenged by a coccidia vaccine to induce NE. Feed intake and body weights were measured on d 8 (NE onset) and end of each feeding period. On d 8, the small intestines of three birds/pen were examined for NE lesions. Jejunum samples and ileal mucosal scrapings from one bird/pen were respectively collected to measure mRNA abundance (d 8 and d 14) and profile the microbiota (d 8 and d 42). Data were analyzed in JMP or QIIME 2 and significance between treatments identified by LSD (P &lt; 0.05). PROB and PPEO had significantly lower mortality (d 0–14) and NE lesion scores compared to NC. Feed conversion ratio was significantly lower in PC, PROB, and PPEO, while average daily gain was higher in PPEO and PC groups compared to NC from d 0–42. On d 8 and d 14, mRNA abundance of claudin-3 was higher in PPEO compared to NC. On d 14, compared to NC, mRNA abundance of sIgA and PGC-1α in PROB and PPEO were lower and higher, respectively. Compared to NC, PPEO increased mTOR abundance on d 14. On d 8, relative abundance of Clostridium sensu stricto 1, Ruminiclostridium9, Prevotellaceae, Prevotellaceae UCG-014, ASF356, and Muribaculaceae was higher in NC compared to PPEO and PROB, while Lactobacillus was lower in NC. Escherichia-Shigella had higher abundance in PC compared to PPEO and PROB. Collectively, these data indicate that during a subclinical naturally occurring NE, supplementation of PROB or PPEO supports performance and reduces intestinal lesions, potentially through modifying tight junction proteins, gut microbiota, immune responses, and cell metabolism.