Submitted to: Experimental Parasitology
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 9/22/2010
Publication Date: 12/19/2010
Citation: Stuard, L.H., Miska, K.B., Jenkins, M.C., Fetterer, R.H., Cox, C.M., Kim, S., Dalloul, R.A. 2010. Expression of innate immunity genes during Eimeria praecox infection in chickens. Experimental Parasitology. 127:714-718. Interpretive Summary: Eimeria praecox represents one of several species of Eimeria that infects chickens resulting in a gastro intestinal disease called coccidiosis. This disease costs the poultry industry billions of dollars in losses worldwide. In the past, E. praecox has been considered to be a minor player in coccidiosis. However recent studies have concluded that this species is very prominent in the field, therefore a better analysis of E. praecox iswarranted. In the current study birds were infected with E. praecox and intestinal samples were taken daily for 7 days. The gene expression profiles in these samples were measured. The study focused on measuring genes that play a role in innate immunity of the chickens. It was found that when the infection load with the parasite was high the expression in these genes was decreased. This finding may be important because a decrease in expression of these genes may render the chicken susceptible to subsequent bacterial infections.
Technical Abstract: Intestinal colonization of avian species by Eimeria parasites results in the enteric disease, coccidiosis. A study was carried out to assess the immunological effects of E. praecox infection on the gut of infected chickens. In experiment 1, birds were orally gavaged with 50,000 E. praecox oocysts; in experiment 2, an infection dosage of 500,000 E. praecox oocysts was used. Duodenal, jejunal, and ileal intestinal sections were sampled consecutively on days 1-7 post-infection. Intestinal expression of innate immune gene transcripts was analyzed by quantitative real-time polymerase chain reaction (qRT-PCR). Analysis of relative gene expression in experiment 1 revealed a decrease (P < 0.05) in Toll-like receptor (TLR)-15 in the duodenum of infected birds on day 2, and an increase on day 6 post-infection. Duodenal expression of TLR3 was significantly upregulated on days 4 and 6 post-infection. On day 3, cathelicidin antimicrobial peptide (CAMP) was downregulated (P < 0.05) in the jejunum of infected chickens. Expression of liver-expressed antimicrobial peptide-2 (LEAP-2) in infected birds was significantly decreased in the duodenum on days 3 and 4, and in the jejunum on day 4. In experiment 2, TLR3 was significantly downregulated on day 7 post-infection in both the duodenum and ileum. A similar pattern was observed in TLR21 and TLR4, with decreased expression (P < 0.05) on day 7 post-infection in the ileum and all three intestinal sections for TLR21 and TLR4, respectively. LEAP-2 was depressed (P < 0.05) on days 3-5 in the duodenum; however, ileal expression was significantly upregulated on day 7. Based on the differing results observed in each experiment, it was concluded that both TLR and antimicrobial peptide expression, and thus immunity may be dependent on infection load.