Expression of Toll-like receptors and antimicrobial peptides during Eimeria praecox infection in XXXX .

@entity308 @entity66 @entity73053 @entity7843 @entity53518 @entity41494 @entity1573 @entity73052 @entity73051
Intestinal colonization of avian species by Eimeria parasites results in the @entity66 , @entity7843 . A study was carried out to assess the immunologic effects of Eimeria praecox infection on the gut of infected @entity1573 . 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 and jejunal 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 an increase (P<0.05) in duodenal Toll-like receptor ( @entity41494 expression on days 4 and 6 post-infection. @entity73051 expression was significantly decreased in the duodenum of infected birds on day 2, and significantly increased on day 6 post-infection. In Experiment 2, @entity41494 was significantly downregulated in the duodenum on day 7 post-infection; however, no significant results were observed in terms of @entity73051 expression. @entity53518 also exhibited decreased expression (P<0.05) on day 7 post-infection in both intestinal sections. Regarding antimicrobial peptide expression; in the first experiment, expression of @entity73052 ( @entity73052 ) in infected birds was significantly decreased in the duodenum on days 3 and 4, and in the jejunum on day 4. Similarly, Experiment 2 resulted in @entity308 of @entity73052 (P<0.05) on days 3-5 in the duodenum. In Experiment 1, cathelicidin antimicrobial peptide ( @entity73053 ) was downregulated (P<0.05) in the jejunum of infected @entity1573 on day 3 post-infection; however, @entity73053 results were non-significant in Experiment 2. 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.
