A temporal investigation of genes associated with intestinal homeostasis in broiler chickens following a single infection with Eimeria acervulina

Authors: CLOFT, SARA - Virginia Tech; Miska, Kate; Jenkins, Mark; KAHL, STANISLAW - Retired ARS Employee; Proszkowiec-Weglarz, Monika; WONG, ERIC - Virginia Tech

Submitted to: Poultry Science
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 1/19/2023
Publication Date: 1/26/2023
Citation: Cloft, S.E., Miska, K.B., Jenkins, M.C., Kahl, S., Proszkowiec-Wegla, M.K., Wong, E.A. 2023. A temporal investigation of genes associated with intestinal homeostasis in broiler chickens following a single infection with Eimeria acervulina. Poultry Science. 102:102537. https://doi.org/10.1016/j.psj.2023.102537.
DOI: https://doi.org/10.1016/j.psj.2023.102537

Interpretive Summary: Coccidiosis is an infectious disease of chickens, and it has a large economic impact on the broiler (meat chicken) industry. The disease is caused by a parasite (Eimeria) that infects the intestinal tract. During the course of infection, the chickens become lethargic, lose appetite, and have diarrhea. These symptoms cause the chickens to not grow as fast as healthy chickens, resulting in monetary losses to the poultry farmer. The purpose of the current study was to investigate the molecules that are associated with immunity and gut health during a two-week period of Eimeria acervulina infection. This species infects the upper regions of the small intestine (duodenum) and the infection peaks around 6 days post infection. It was found that the E. acervulina infection caused decrease in expression of molecules related to immunity (defensins) and gut health (mucin), suggesting that the infection might decrease the effectiveness of the immune response against the parasite, and affect the integrity of the gut. It was also observed that molecules that have a role in cell proliferation and development were increased during infection, which suggest that the intestine undergoes a period of repair after infection and replaces infected cells with new healthy cells. This research furthers our understanding of the effects of Eimeria infection on broiler chickens. By understanding these effects, new therapies can be investigated in the future.

Technical Abstract: Infection with the protozoan parasite Eimeria causes the economically devastating disease coccidiosis, which is characterized by gross tissue damage and inflammation resulting in blunted villi and altered intestinal homeostasis. Broiler chickens at 21 days 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 days post-infection (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 Eimeria 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 Eimeria 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 from the loss of Muc2 in the localized regions where the Eimeria had invaded the tissue.