Down Regulation of Colon Mucin Production Induced by Eimeria pragensis Infection

Eimeria pragensis, an intestinal protozoa infecting mice, induces colitis and reduces goblet cell numbers in the large intestine. In the present study, we investigated the pathogenesis and the mechanisms underlying goblet cell down-regulation in the early phase of infection. Male C57BL6 mice were orally infected with 300 oocysts. Colon tissues were collected at 0(control), 3, 8, and 13 days post-infection(dpi). To elucidate mechanisms of goblet cell dysfunction, we performed RNA sequencing of large intestine tissue to examine host as well as parasite transcriptomes. RNA sequencing of infected large intestines revealed that E. pragensis produced enzymes that were known to degrade mucin and tight junctions, and proteins that could activate the NotchHes1 signaling pathway. As for host responses, genes associated with Th1type inflammation, epithelial barrier disruption, and immune regulation were up-regulated as early as 3 dpi. These results suggested that E. pragensis infection induces a mucosal barrier dysfunction in the early phase of the infection, which possibly causes the tissue invasion of bacteria in the large intestine. Th1type inflammatory response, thus induced, reduces goblet cell numbers and mucin production. This model provides valuable insight into the mechanisms of mucosal barrier disruption during protozoan infection.