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ARS Home » Northeast Area » Beltsville, Maryland (BARC) » Beltsville Agricultural Research Center » Animal Parasitic Diseases Laboratory » Research » Publications at this Location » Publication #314745

Research Project: DEVELOPMENT OF CONTROL AND INTERVENTION STRATEGIES FOR AVIAN COCCIDIOSIS

Location: Animal Parasitic Diseases Laboratory

Title: Expression of an antimicrobial peptide, digestive enzymes and nutrient transporters in the intestine of E. praecox-infected chickens

Author
item Yin, H - Virginia Polytechnic Institution & State University
item Sumners, Lindsay - Virginia Polytechnic Institution & State University
item Dalloul, Rami - Virginia Polytechnic Institution & State University
item Miska, Kataryzyna - Virginia Polytechnic Institution & State University
item Fetterer, Raymond
item Jenkins, Mark
item Zhu, Q - Virginia Polytechnic Institution & State University
item Wong, Eric - Virginia Polytechnic Institution & State University

Submitted to: Poultry Science
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 4/16/2015
Publication Date: 5/26/2015
Citation: Lin, H., Summers, L., Dalloul, R., Miska, K., Fetterer, R.H., Jenkins, M.C., Zhu, Q., Wong, E. 2015. Expression of an antimicrobial peptide, digestive enzymes and nutrient transporters in the intestine of E. praecox-infected chickens. Poultry Science. 94:1521-1526.

Interpretive Summary: Poultry coccidiosis is an intestinal disease caused by several different species of a protozoan intestinal parasite which causes considerable annual losses to the poultry industry. The primary control for the disease is through applied medications in the feed as birds are raised in confinement in broiler houses. The control by medications is becoming less effective because of increased resistance to the drugs and less desirable due to concerns about the possibility of drugs remaining in the meat and within the environment. Coccidiosis interferes with maintenance of healthy nutrition during poultry production by producing lesions in cells of the small intestine. The current study is a continuation of a long term project focused on how a coccidia infection changes molecules in the intestine that transport nutrients (sugars and amino acids) from the gut to be used by the organism. The objective of this study was to examine changes in expression of digestive enzymes, nutrient transporters and an antimicrobial peptide following an infection of chicks with Eimeria praecox a coccidian parasite of the small intestine. These results were compared with findings from other coccidian species. In the anterior part of small intestine, the primary site of E. praecox infection, the expression of a number of genes involved in nutrient absorption and an antimicrobial peptide was decreased. In the middle and the end regions of the small intestine, decreases in expression of some of these genes were noted even though there is little direct invasion of these regions of the intestine by the parasite. The decreases in gene expression observed in the current study are similar to those observed in previous studies using other species of coccidian. Together these observations suggest a common cellular response to coccidia infection.

Technical Abstract: Coccidiosis is a major intestinal disease of poultry, caused by several species of the protozoan Eimeria. The objective of this study was to examine changes in expression of digestive enzymes, nutrient transporters and an antimicrobial peptide following an Eimeria praecox challenge of chickens at days 3 and 6 post-infection. In the duodenum, the primary site of E. praecox infection, a number of genes were downregulated at both d3 and d6 post-infection. These genes included liver expressed antimicrobial peptide 2 (LEAP2), the cationic (CAT1), anionic (EAAT3), and L-type (LAT1) amino acid transporters, the peptide transporter PepT1 and the zinc transporter ZnT1. Other transporters were downregulated either at d3 or d6. In the jejunum, there was downregulation of BoAT and CAT1 at both d3 and d6; while in the ileum there was downregulation of LEAP2 and LAT1 at both d3 and d6. LEAP2, EAAT3 and ZnT1 have been found to be downregulated following challenge with other Eimeria species, suggesting a common cellular response to Eimeria.