Abstract
Simple SummaryEimeria-induced coccidiosis, a common disease in the poultry industry, causes substantial economic loss globally. The developed resistance to synthetic anticoccidial drugs and increasing public and legislative pressures to decrease antibiotic utilization drive research exploring non-antibiotic alternatives to control coccidiosis. Two experiments were conducted to investigate the potential mechanisms by which enzymes may mitigate the negative effects of Eimeria on growth performance, nutrient-transporter gene expression, and cecal fermentation patterns. The results demonstrated that Eimeria changed the expression of tight junctions and nutrient transporters genes, promoted cecal protein fermentation, and inhibited cecal saccharolytic fermentation. Exogenous xylanase and protease supplementation alleviated negative effects of Eimeria effects on the above responses, and thus demonstrated benefits of enzyme supplementation beyond improvement in nutrient utilization. Two 21-day experiments were conducted to investigate the effects of exogenous enzymes on growth performance, tight junctions, and nutrient transporters, jejunal oligosaccharides and cecal short-chain fatty acids (SCFA) of broiler chickens challenged with mixed Eimeria. Two different basal diets: high fiber-adequate protein (HFAP; Expt. 1) or low fiber-low protein (LFLP; Expt. 2) were used in the two experiments. In each experiment, birds were allocated to four treatments in a 2 × 2 factorial arrangement (with or without protease and xylanase combination; with or without Eimeria challenge). In Expt. 1, with HFAP diets, Eimeria upregulated (p < 0.05) the expression of claudin-1, but downregulated (p < 0.05) glucose transporters GLUT2/GLUT5. On the contrary, enzymes downregulated (p < 0.05) claudin-1 and alleviated the Eimeria-depressed GLUT2/GLUT5 expression. In both experiments, Eimeria decreased (p < 0.05) cecal saccharolytic SCFA and increased (p < 0.05) cecal branched-chain fatty acids. The challenge × enzyme interaction (p < 0.05) showed that enzymes reversed the Eimeria effects on fermentation pattern shift. In conclusion, Eimeria altered tight junctions and nutrient transporters expression promoted cecal proteolytic fermentation and inhibited saccharolytic fermentation. Exogenous enzymes showed the potential of alleviating the Eimeria-induced intestinal gene expression changes and reversing the unfavorable cecal fermentation pattern.
Highlights
Avian coccidiosis is a worldwide disease that is caused by protozoan parasites of Eimeria spp
Seven species of Eimeria including E. acervuline, E. brunetti, E. maxima, E. mitis, E necatrix, E. praecox, and E. tenella have been identified in the broiler chicken industry [1]
In both Expt. 1 and 2, Eimeria challenge resulted in a significant reduction (p < 0.01) in weight gain (WG), feed intake (FI), and gain–feed ratio (Tables 4 and 5)
Summary
Avian coccidiosis is a worldwide disease that is caused by protozoan parasites of Eimeria spp. The prevalence of coccidiosis usually occurs with a mixed infection instead of a single species with the mixed infection by E. acervulina, E. maxima, and E. tenella being more prevalent [2]. These three species of Eimeria spp. preferentially invade and multiply in the regions of duodenum, jejunum plus ileum, and ceca, respectively; intersectional infection can be observed [3]. The changes to intestinal nutrient transporters including sugars, amino acids, and mineral transporters may partly contribute to the Eimeria-induced growth depression [6,7]. It has been demonstrated that Eimeria infection impacted the microbial population and composition in the hindgut of broiler chickens, resulting in cecal dysbacteriosis. The dysbacteriosis in the hindgut indicates a shift of fermentation patterns in ceca
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