Abstract
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► Rabbit coccidiosis caused by Eimeria coecicola. ► Structural reorganizations in the non-target spleen. ► Deregulation of gene expression in spleen. ► Granzyme H expressing NK cells possibly involved in host response.
The apicomplexan protozoon Eimeria coecicola is an infectious agent of intestinal coccidiosis in rabbits, causing severe injuries in the appendix as the final target, but also in the liver though not being a target. Here, we investigated the effect of E. coecicola on the spleen of the rabbit Oryctolagus cuniculus with respect to structure and gene expression using 2-color Agilent whole rabbit genome oligo-microarray technology in combination with quantitative PCR. At maximal fecal output of E. coecicola oocyts on day 7p.i., the spleen did not contain any parasites, but displayed moderate inflammatory changes evidenced as fused white pulp areas, diffuse appearance of the marginal zones, and increased number of macrophages in the red pulp, eventually resulting in an increased histological score. The infections induced 36 genes to be up-regulated and 156 genes to be down-regulated, among which were 139 genes encoding diverse regions of antibodies. The highest upregulated genes were those encoding granzyme H (10-fold), lim1 (10-fold), xanthine dehydrogenase (9-fold), whereas the downregulated genes could be majorly assigned to the immune response, as e.g. the genes encoding the macrophage cationic peptide-2 (5-fold). Quantitative PCR of genes encoding GZMH, XDH, HSD17B1, SULT3A1, SAA, BPI, MCP-2, and GST exhibited the same transcriptional level as that detected by microarray analysis. The E. coecicola-induced changes in gene expression of the spleen were totally different to those found previously in appendix and liver. Only the granzyme H gene became upregulated in all three organs. Our data indicate that the spleen, though not a final target of E. coecicola, responds to E. coecicola infections, suggesting that the spleen may be part of an orchestrated host defense against E. coecicola critically involving GZMH-expressing NK-cells.