Location: Animal Parasitic Diseases LaboratoryTitle: Expression of digestive enzymes and nutrient transporters in Eimeria-challenged broilers
|SU, SHENGCHEN - Virginia Polytechnic Institution & State University|
|WONG, ERIC - Virginia Polytechnic Institution & State University|
Submitted to: Experimental Parasitology
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 1/7/2015
Publication Date: 3/20/2015
Citation: Su, S., Miska, K.B., Fetterer, R.H., Jenkins, M.C., Wong, E. 2015. Expression of digestive enzymes and nutrient transporters in Eimeria-challenged broilers. Experimental Parasitology. 150:13-21.
Interpretive Summary: Chicken is the most widely consumed meat in the United States, and it is projected that by 2020 it will be the most widely consumed meat worldwide. Compared to beef and pork, chicken is relatively inexpensive to produce. The largest cost of raising chickens is feed, therefore maintaining chickens in an environment that supports proper nutrition is essential. In large-scale poultry productions, parasitic diseases that affect intestinal health and interfere with maintaining healthy nutrition are common. When infected chickens fail to gain weight and exhibit decreased feed efficiency. One of the most common species of single cell parasites that infect different regions of the gut is Eimeria. The current study focuses on how Eimeria infection changes molecules in the intestine that transport nutrients (sugars and amino acids) from the gut to be used by the organism. It was found that all three species of Eimeria investigated changes the expression of these molecules in the small as well as large intestine. In most cases a decrease in expression of these molecules was observed (but in a few cases the molecules increased in expression). All three species of parasite tested resulted in reduced expression of a molecule called LEAP2. This molecule is associated with anti-microbial activity, therefore the reduced expression could result lowering of the immune response of the infected chickens to bacteria. The decrease in the number of nutrient transporters during infections could at least in part explain the reason why infected chickens gain weight more slowly than healthy birds. More work is necessary to investigate the how Eimeria parasites alter nutrient use in chicken so that possible feeding strategies could be designed to help control the infection quickly.
Technical Abstract: Avian coccidiosis is a disease caused by the intestinal protozoa Eimeria. The site of invasion and lesions in the intestine is species-specific, for example E. acervulina affects the duodenum, E. maxima the jejunum, and E. tenella the ceca. Lesions in the intestinal mucosa cause reduced feed efficiency and body weight gain. The 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 compare the expression of digestive enzymes, nutrient transporters and an antimicrobial peptide in broilers challenged with either E. acervulina, E. maxima or E. tenella. The genes examined included digestive enzymes (APN and SI), peptide and amino acid transporters (PepT1, ASCT1, bo,+AT/rBAT, B0AT, CAT1, CAT2, EAAT3, LAT1, y+LAT1 and y+LAT2), sugar transporters (GLUT1, GLUT2, GLUT5 and SGLT1), zinc transporter (ZnT1) and an antimicrobial peptide (LEAP2). Duodenum, jejunum, ileum and ceca were collected seven days post challenge. E. acervulina challenge resulted in downregulation of various nutrient transporters or LEAP2 in the duodenum and ceca, but not the jejunum or ileum. E. maxima challenge produced both downregulation and upregulation of nutrient transporters and LEAP2 in all three segments of the small intestine and ceca. E. tenella challenge resulted in the downregulation and upregulation of nutrient transporters and LEAP2 in the jejunum, ileum and ceca, but not the duodenum. At the respective target tissue, E. acervulina, E. maxima and E. tenella infection caused common downregulation of APN, bo,+AT, rBAT, EAAT3, SI, GLUT2, GLUT5, ZnT1 and LEAP2. The downregulation of nutrient transporters would result in a decrease in the efficiency of protein and polysaccharide digestion and uptake, which may partially explain the weight loss depression. The downregulation of nutrient transporters may also be a cellular response to reduced expression of the host defense protein LEAP2, which would diminish intracellular pools of nutrients and inhibit pathogen replication.