Su S, Miska K B, Fetterer R H, Jenkins M C, Wong E A
Department of Animal and Poultry Sciences, Virginia Tech, Blacksburg, VA 24061, USA.
Animal Biosciences and Biotechnology Laboratory, USDA/ARS, Beltsville, MD, USA.
Exp Parasitol. 2015 Mar;150:13-21. doi: 10.1016/j.exppara.2015.01.003. Epub 2015 Jan 21.
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, b(0,+)AT/rBAT, B(0)AT, 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 7 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, b(0,+)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. 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.
禽球虫病是一种由肠道原生动物艾美耳球虫引起的疾病。肠道内的侵袭部位和病变具有种特异性，例如堆型艾美耳球虫感染十二指肠，巨型艾美耳球虫感染空肠，柔嫩艾美耳球虫感染盲肠。肠道黏膜的病变会导致饲料效率和体重增加降低。生长减缓可能是由于肠道中消化酶和营养转运蛋白表达的变化。本研究的目的是比较感染堆型艾美耳球虫、巨型艾美耳球虫或柔嫩艾美耳球虫的肉鸡中消化酶、营养转运蛋白和一种抗菌肽的表达。检测的基因包括消化酶（氨肽酶N和蔗糖酶异麦芽糖酶）、肽和氨基酸转运蛋白（肽转运蛋白1、中性氨基酸转运蛋白1、b(0,+)型氨基酸转运蛋白/肾性氨基酸转运蛋白、B(0)型氨基酸转运蛋白、阳离子氨基酸转运蛋白1、阳离子氨基酸转运蛋白2、兴奋性氨基酸转运体3、L型氨基酸转运蛋白1、y(+)L型氨基酸转运蛋白1和y(+)L型氨基酸转运蛋白2）、糖转运蛋白（葡萄糖转运蛋白1、葡萄糖转运蛋白2、葡萄糖转运蛋白5和钠葡萄糖协同转运蛋白1）、锌转运蛋白（锌转运体1）和一种抗菌肽（肝脏表达抗菌肽2）。攻毒后7天收集十二指肠、空肠、回肠和盲肠。感染堆型艾美耳球虫导致十二指肠和盲肠中各种营养转运蛋白或肝脏表达抗菌肽2下调，但空肠或回肠未出现这种情况。感染巨型艾美耳球虫导致小肠和盲肠所有三个节段的营养转运蛋白和肝脏表达抗菌肽2既有下调也有上调。感染柔嫩艾美耳球虫导致空肠、回肠和盲肠中营养转运蛋白和肝脏表达抗菌肽2下调和上调，但十二指肠未出现这种情况。在各自的靶组织中，感染堆型艾美耳球虫、巨型艾美耳球虫和柔嫩艾美耳球虫均导致氨肽酶N、b(0,+)型氨基酸转运蛋白、肾性氨基酸转运蛋白、兴奋性氨基酸转运体3、蔗糖酶异麦芽糖酶、葡萄糖转运蛋白2、葡萄糖转运蛋白5、锌转运体1和肝脏表达抗菌肽2共同下调。营养转运蛋白的下调会导致蛋白质和多糖消化及吸收效率降低，这可能部分解释了体重减轻的原因。营养转运蛋白的下调也可能是细胞对宿主防御蛋白肝脏表达抗菌肽2表达降低的一种反应，这会减少细胞内营养物质池并抑制病原体复制。
