Sodium bisulfate (SB) was evaluated on its ability to improve broiler growth and intestinal structure with(out) a coccidia challenge. One thousand two hundred Cobb500 day-old males were randomly assigned within 4 experimental groups with a 2 × 2 factorial design, with (out) SB in the diet and with(out) a day 0 coccidia challenge using a 10× dose of a commercial vaccine. At day 7, oocysts per gram of feces were determined. At day 0, 14, 28, and 41, BW and feed consumption were measured. At day 21, 20 birds per treatment were subjectively scored for coccidia lesions, and jejunal histologic samples were collected for villi measurements. Twenty additional birds were given fluorescein isothiocyanate-dextran to determine gut permeability. At day 41, 10 birds per treatment had histologic samples collected. Statistical analysis was conducted in JMP Pro 14 using GLM procedure to compare disease state and diet. Means were separated using Dunnett's test (P ≤ 0.05) with the nonchallenged standard diet treatment that is cllenged control had a larger apical width (P = 0.03) and thicker muscularis (P = 0.04) on day 41. Overall, the addition of SB during coccidial enteropathy aided in BW, feed conversion ratio, and villi health with no observed effects on parasite cycling.This study investigated the effects of a Lactobacillus paracasei KL1 and Lactobacillus plantarum subsp. plantarum Zhang-LL mixed probiotic on Salmonella-caused pullorosis in chicks. A total of 120 1-day-old Nongda no.3 dwarf chicks were randomly assigned to 4 treatments, with 6 replicates of 5 birds each. The treatments were blank group, Salmonella pullorum-infected group, probiotic treatment group, and probiotic prevention (PP) group. All birds (n = 90) except those in the blank group were infected with S. pullorum on day 4. On day 14, the BW, ADG, mortality, pathology of tissue, cecum colony count, immune organ indices, cecal mucosa secretory IgA, and cytokines were investigated. The results showed that the chicks infected with S. pullorum were depressed and their BW reduced. The PP group had the highest ADG and lowest mortality rate (0%), whereas the S. pullorum-infected group had 37.50% mortality rate and lowest ADG.  https://www.selleckchem.com/  Pathologic sections showed that the probiotic treatment group had minor lesions but the PP group had no lesions in the ileum, cecum, and liver. Cecal Lactobacillus counts was the highest (P 0.05) in the bursa of Fabricius, whereas in the PP group, all the immune organs were increased (P less then 0.05).Cecal mucosa secretory IgA and IL-4 were the highest (P less then 0.05) and tumor necrosis factor α and interferon gamma were the lowest (P less then 0.05) in the PP group; In summary, the Lactobacillus KL1 and L. plantarum Zhang-LL mixed probiotic effectively reduced the mortality of pullorosis in chicks, promoted the growth performance, regulated the balance of the intestinal flora, improved the immune function, resisted pullorosis disease, completely prevented chicks from pullorosis after infection, and reduced economy loss in the poultry industry.Nutraceuticals are not only nutritionally beneficial for animals but also their use as feed supplements may reduce environmental contamination. The effect of fermented defatted "alperujo," an olive oil by-product, supplementation on the intestinal health of broiler chickens was assessed by analyzing the intestinal mucosal morphology of the duodenum and the cecum. The microbiota of the cecum was also characterized by analyzing the V3-V4 region of the 16S rRNA gene on days 7, 14, 21, 28, 35, and 42. Supplemented broilers from 14 to 35 D of age showed an increase in villus height in the duodenum. This increase likely improved digestibility and absorption capacity during growth, leading to the observed increase in BW at day 35 of life. A progressive increase in crypt depth in both the duodenum and the cecum was also observed. This modification likely enhanced epithelial renewal, thus safeguarding the turnover capacity of the intestinal mucosa. Our molecular analysis of cecal microbiota suggests that this dietary supplement may favor the growth of certain bacteria and may control the spread of pathogenic bacteria by means of competitive exclusion.Overfeeding causes severe steatosis but not inflammation in goose liver, suggesting existence of protective components. Previous studies have shown that some intestinal microbes and their metabolites damage intestinal structural integrity and function, thus causing inflammation in the development of human and mouse nonalcoholic fatty liver disease. Therefore, this study hypothesizes that intestinal structural integrity of goose is maintained during overfeeding, which may provide goose fatty liver a protective mechanism against inflammation. To test this hypothesis, 48 seventy-day-old healthy Landes male geese were overfed (as overfeeding group) or normally fed (as control group). Blood and intestine (jejunum, ileum, and cecum) samples were harvested on the 12th and 24th d of overfeeding. Data showed that goose fatty liver was successfully induced by 24 d of overfeeding. Hematoxylin-eosin staining analysis indicated that the arrangement of villi and crypts in the intestine was orderly, and the intestinal structure was intact with no pathological symptoms in the 2 groups. Enzyme-linked immunosorbent assay and quantitative PCR analysis indicated no significant differences in the expression of tight junction and inflammation-related genes as well as plasma lipopolysaccharide concentration between the groups. Ileal hypertrophy and cecal atrophy were observed in the overfed vs. control geese, probably because of change of sphingolipid metabolism. Activation of apoptotic pathway may help cecum avoid necrosis-induced inflammation. In conclusion, healthy and intact intestine provides a layer of protection for goose fatty liver against inflammation. Sphingolipid metabolism may be involved in the adaptation of ileum and cecum to overfeeding. The hypertrophy of ileum makes it an important contributor to the development of goose fatty liver. The atrophy and decline in the function of cecum may be caused by apoptosis induced by overfeeding.