Cryptosporidial Infection Suppresses Intestinal Epithelial Cell MAPK Signaling Impairing Host Anti-Parasitic Defense

Cryptosporidium is a genus of protozoan parasites that infect the gastrointestinal epithelium of a variety of vertebrate hosts. Intestinal epithelial cells are the first line of defense and play a critical role in orchestrating host immunity against Cryptosporidium infection. To counteract host defense response, Cryptosporidium has developed strategies of immune evasion to promote parasitic replication and survival within epithelial cells, but the underlying mechanisms are largely unclear. Using various models of intestinal cryptosporidiosis, we found that Cryptosporidium infection caused suppression of mitogen-activated protein kinase (MAPK) signaling in infected murine intestinal epithelial cells. Whereas expression levels of most genes encoding the key components of the MAPK signaling pathway were not changed in infected intestinal epithelial cells, we detected a significant downregulation of p38/Mapk, MAP kinase-activated protein kinase 2 (Mk2), and Mk3 genes in infected host cells. Suppression of MAPK signaling was associated with an impaired intestinal epithelial defense against C. parvum infection. Our data suggest that cryptosporidial infection may suppress intestinal epithelial cell MAPK signaling associated with the evasion of host antimicrobial defense.

Prevalence of cryptosporidial infection in piglets with clinical signs of enterophaty

In our examination cryptosporidial infections were detected in the 12,84% (69/537) of examined pigs. Organisms were found in the microvillus brush in the ileum, jejunum rarely in colon. The fact that 78% of those infected were 11-12 weeks old would suggest that there was a strong possibility of sub clinical infection in the weaned pig. All of cryptosporidia infected pigs had diarrhea but 32% of these had other primary diarrheagenic agents which also suggested that diarrhea in farm breeding pigs is a multifactor problem and cryptosporidia may act in concert with other agents to induce of exacerbate the clinical disease.