Location: Animal Parasitic Diseases
Title: Expression of digestive enzymes and nutrient transporters in Eimeria acervulina-challenged layers and broilers Authors
Submitted to: Poultry Science
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: February 20, 2014
Publication Date: May 12, 2014
Repository URL: http://ps.oxfordjournals.org/content/93/5/1217.full.pdf
Citation: Su, S., Miska, K.B., Fetterer, R.H., Jenkins, M.C., Wong, E. 2014. Expression of digestive enzymes and nutrient transporters in Eimeria acervulina-challenged layers and broilers. Poultry Science. 95:1217-1226. Interpretive Summary: Poultry coccidiosis is caused by several different species of an intestinal protozoan parasite which causes considerable annual losses to the poultry industry. The primary impact of coccidiosis on the chicken is reduced growth and decreased feed efficiency. This growth reduction may result from changes in expression of genes regulating digestive enzymes and nutrient transporter molecules on membranes of cells located on the absorptive surface of the intestine. The objective of the study was to determine the expression of these genes in the intestinal tract of both broiler and layer breeds of chickens infected with a parasite species that infects the upper digestive tract. The results indicate that the expression of 10 of 12 genes studied was significantly decreased in the upper digestive tract of both infected broiler and layer chicks compared to uninfected chickens. This change may be the result of damage of intestinal cells caused by the invading parasite. In layer chicks, the expression of genes regulating nutrient absorption were decreased in the lower part of the intestine even though the parasite does not invade cells in this area of the gut. In contrast, the gene expression in the lower part of the intestine of broiler chicks was unchanged. Broiler and layer breeds have been selected over many generations to maximize egg production and for rapid growth respectively. These genetic differences may account for the different response in gene expression observed in the two breeds. The results of the study also indicate that expression of nutrient transporters is decreased during infection in both breeds.
Technical Abstract: Avian coccidiosis is a disease caused by the intestinal protozoa Eimeria. Eimeria-infected chickens develop lesions in the intestinal mucosa, which result in reduced feed efficiency and body weight gain. This growth reduction may be due to changes in expression of digestive enzymes and nutrient transporters in the intestine. The objective of this study was to examine the expression of digestive enzymes, transporters of amino acids, peptides, sugars and minerals, and an antimicrobial peptide in the duodenum, jejunum, and ileum of E. acervulina-infected broilers and layers. In the duodenum, which is the target tissue for E. acervulina, there was downregulation of aminopeptidase N (APN), sucrase-isomaltase, the neutral amino acid transporter B0AT, anionic amino acid transporter EAAT3, the cationic amino acid transporter CAT2, the sugar transporter GLUT2, the zinc transporter ZnT1, and the antimicrobial peptide LEAP2. In the jejunum of layers there was downregulation of many of the same genes as in the duodenum plus downregulation of the peptide transporter PepT1, the Na+-independent neutral/cystine, cationic amino acid exchanger bo,+AT/rBAT, and the y+ L amino acid transporters-1 and 2 (y+ LAT1, y+ LAT2). In the ileum of layers there was downregulation of CAT2, y+LAT1, the L type amino acid transporter LAT1 and the sugar transporter GLUT1, and upregulation of APN, PepT1, the sodium glucose transporter SGLT4 and LEAP2. In E. acervulina infected broilers, there were no gene expression changes in the jejunum and ileum. The jejunum and ileum of broilers is less susceptible to changes in gene expression resulting from E. acervulina infection. These changes in intestinal digestive enzyme and nutrient transporter gene expression may result in a decrease in the efficiency of protein digestion, uptake of essential amino acids and the energy source (glutamate), and disruption of mineral balance. This may ultimately lead to cell death and may be part of the host defense mechanism for eliminating infected cells and inhibition of pathogen replication.