School of Animal Sciences, Virginia Tech, Blacksburg, VA 24061, USA.
Animal Biosciences and Biotechnology Laboratory, Henry A. Wallace Beltsville Agricultural Research Center, Beltsville, MD 20705, USA.
Poult Sci. 2023 Apr;102(4):102537. doi: 10.1016/j.psj.2023.102537. Epub 2023 Jan 26.
Infection with the protozoan parasite Eimeria can cause the economically devastating disease coccidiosis, which is characterized by gross tissue damage and inflammation resulting in blunted villi and altered intestinal homeostasis. Male broiler chickens at 21 d of age were given a single challenge with Eimeria acervulina. Temporal changes in intestinal morphology and gene expression were investigated at 0, 3, 5, 7, 10, and 14 d postinfection (dpi). There were increased crypt depths for chickens infected with E. acervulina starting at 3 dpi and continuing to 14 dpi. At 5 and 7 dpi, infected chickens had decreased Mucin2 (Muc2), and Avian beta defensin (AvBD) 6 mRNA at 5 and 7 dpi and decreased AvBD10 mRNA at 7 dpi compared to uninfected chickens. Liver-enriched antimicrobial peptide 2 (LEAP2) mRNA was decreased at 3, 5, 7, and 14 dpi compared to uninfected chickens. After 7 dpi, there was increased Collagen 3a1 and Notch 1 mRNA compared to uninfected chickens. Marker of proliferation Ki67 mRNA was increased in infected chickens from 3 to 10 dpi. In addition, the presence of E. acervulina was visualized by in situ hybridization (ISH) with an E. acervulina sporozoite surface antigen (Ea-SAG) probe. In E. acervulina infected chickens, Ea-SAG mRNA was only detectable on 5 and 7 dpi by both ISH and qPCR. To further investigate the site of E. acervulina infection, Ea-SAG and Muc2 probes were examined on serial sections. The Muc2 ISH signal was decreased in regions where the Ea-SAG ISH signal was present, suggesting that the decrease in Muc2 by qPCR may be caused by the loss of Muc2 in the localized regions where the E. acervulina had invaded the tissue. Eimeria acervulina appears to manipulate host cells by decreasing their defensive capabilities and thereby allows the infection to propagate freely. Following infection, the intestinal cells upregulate genes that may support regeneration of damaged intestinal tissue.
感染原生动物寄生虫艾美耳球虫会导致具有经济破坏性的疾病球虫病，其特征是组织严重损伤和炎症，导致绒毛变钝和肠道内稳态改变。21 日龄雄性肉鸡接受艾美耳属球虫单一攻毒。在感染后 0、3、5、7、10 和 14 天，研究了肠道形态和基因表达的时间变化。感染艾美耳属球虫的鸡从 3 天开始，一直到 14 天，隐窝深度增加。在 5 和 7 天，感染鸡的黏蛋白 2（Muc2）和禽类β防御素（AvBD）6mRNA 减少，而 7 天感染鸡的 AvBD10mRNA 减少与未感染鸡相比。与未感染鸡相比，肝富集抗菌肽 2（LEAP2）mRNA 在 3、5、7 和 14 天减少。感染后 7 天，与未感染鸡相比，Collagen3a1 和 Notch1mRNA 增加。感染鸡的增殖标志物 Ki67mRNA 从 3 天到 10 天增加。此外，用艾美耳属球虫孢子表面抗原（Ea-SAG）探针的原位杂交（ISH）可观察到艾美耳属球虫的存在。在感染艾美耳属球虫的鸡中，通过 ISH 和 qPCR 仅在 5 和 7 天可检测到 Ea-SAGmRNA。为了进一步研究艾美耳属球虫感染的部位，在连续切片上检查了 Ea-SAG 和 Muc2 探针。Ea-SAGISH 信号存在的区域，Muc2ISH 信号减少，表明 qPCR 中 Muc2 的减少可能是由于 Muc2 在艾美耳属球虫侵入组织的局部区域丢失所致。艾美耳属球虫似乎通过降低宿主细胞的防御能力来操纵宿主细胞，从而使感染自由传播。感染后，肠道细胞上调可能支持受损肠道组织再生的基因。
