Effect of IL-10 and IL-6 on the regulation of hepcidin in (a) primary macrophages and (b) HepG2 cells. Data show fold-increase relative to mRNA in media control.

<p>Error bars indicate standard error of the mean. Bar plots show data from at least 3 independent experiments. ** <i>P</i><0.01, ***<i>P</i><0.001 (Mann-Whitney test, compared with Media control).</p

Proposed model of hepcidin in malaria infection.

<p>The regulation of hepcidin in response to infection may vary with cell type. A major response to infection occurs in hepatocytes in response to IL-6. However, our observations support the role of IL-10 in primary macrophages. Availability of iron to erythroid developing cells ultimately depends on macrophages and thus the high concentration of IL-10 may play a key regulatory role. Indeed, actively dividing cells like those found in the bone marrow are more susceptible to oxidative damage. In this context, both the direct anti-inflammatory effect of IL-10 and its indirect effect on iron restriction through the up-regulation of hepcidin may be beneficial.</p

Long untranslated regions and putative anti-sense non-coding RNAs in <i>Tg</i>VEG and <i>Nc</i>LIV.

<p>(A) Length distribution of 5’UTRs, 3’UTRs and CDS in <i>Toxoplasma gondii</i>, <i>Neospora caninum</i>, <i>Schizosaccharomyces pombe</i>, <i>Arabidopsis thaliana</i>, <i>Caenorhabditis elegans</i>, <i>Drosophila melanogaster</i> and <i>Homo sapiens</i>. 5’UTRs are found to be strikingly large in the parasites, almost 4 times higher than other eukaryotes. 3’UTRs are comparable to those in human and longer than other eukaryotes. (B) Sequence conservation across UTRs and their flanking intergenic regions. UTR regions are generally more conserved than their flanking intergenic regions. (C) Log abundance ratio of antisense non-coding RNA (ancRNA) and sense coding mRNA pair versus sense coding RNA. There is an inverse relation between abundances of ancRNA and their sense mRNA counterpart.</p

Summary of the manually curation of <i>Tg</i>VEG and <i>Nc</i>LIV (ToxoDb v8.0) genes.

<p>A gene model was “corrected” by adding/deleting exons or altering their exon-intron boundaries to conform to the transcript and peptide evidence. The corrected genes also include the models that were either “split” into two separate genes or “merged” into a single gene based on transcript splice-site evidence. “New” genes were annotated in open reading frames with clear expression evidence. Genes that lacked expression evidence and overlapped with an expressed gene model were considered spurious and “deleted”.</p