Abstract
Although IL17A is associated with the immunological control of various infectious diseases, its role in host response to Eimeria infections is not well understood. In an effort to better dissect the role of IL17A in host-pathogen interactions in avian coccidiosis, a neutralizing antibody (Ab) to chicken IL17A was used to counteract IL17A bioactivity in vivo. Chickens infected with Eimeria tenella and treated intravenously with IL17A Ab, exhibited reduced intracellular schizont and merozoite development, diminished lesion score, compared with untreated controls. Immunohistological evaluation of cecal lesions in the parasitized tissues indicated reduced migration and maturation of second-generation schizonts and reduced lesions in lamina propria and submucosa. In contrast, untreated and infected chickens had epithelial cells harboring second-generation schizonts, which extend into the submucosa through muscularis mucosa disruptions, maturing into second generation merozoites. Furthermore, IL17A Ab treatment was associated with increased parameters of Th1 immunity (IL2- and IFNγ- producing cells), reduced levels of reactive oxygen species (ROS), and diminished levels of serum matrix metalloproteinase-9 (MMP-9). Finally, schizonts from untreated and infected chickens expressed S100, Wiskott-Aldrich syndrome protein family member 3 (WASF3), and heat shock protein-70 (HSP70) proteins as merozoites matured, whereas the expression of these proteins was absent in IL17A Ab-treated chickens. These results provide the first evidence that the administration of an IL17A neutralizing Ab to E. tenella-infected chickens inhibits the migration of parasitized epithelial cells, markedly reduces the production of ROS and MMP-9, and decreases cecal lesions, suggesting that IL17A might be a potential therapeutic target for coccidiosis control.
Highlights
The coccidial parasite, Eimeria tenella, is a significant cause of intestinal disease in chickens and hens worldwide
Effect of IL17A Ab on schizont migration through the cecal wall At day 5 pi, when large numbers of schizonts are present in the cecal mucosa, fibronectin-expressing schizonts were identified as they migrated from the epithelial lining of the crypts of Lieberkühn through the cecal wall (Figures 2A and 2B)
IL17A is known to be involved in the host response to protozoal infections [7,9], and its production has been associated with the protective response to coccidial infections [25], the specific effect of IL17A on E. tenella infection has not been clearly defined
Summary
The coccidial parasite, Eimeria tenella, is a significant cause of intestinal disease in chickens and hens worldwide. Eimeria tenella is an intracellular obligate protozoan parasite having a complex life cycle of seven days, during which it undergoes intracellular development and proliferates through characteristic intracellular stages confined to the cecal epithelium. Eimeria tenella initially invades the epithelial cells lining in the lumen of the crypts of Lieberkhün. The ensuing life cycle of the parasite involves detachment of the parasitized cells from the epithelial layer and their migration to the underlying connective tissue of the lamina propria (LP), where maturation to schizonts occurs [1]. The ability of parasitized epithelial cells to detach from the epithelium lining of the crypts, migrate through the basal membrane underneath the epithelium, and invade the LP relies on a complex cascade of molecular events involving a finely tuned interplay between parasite and host cells. IL17A induces the production of reactive oxygen species (ROS) [10], and activates the epithelial cell contractile machinery through cytoskeleton rearrangements del Cacho et al Veterinary Research 2014, 45:25 http://www.veterinaryresearch.org/content/45/1/25
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