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<i>Cryptosporidium</i> spp. are enteric protozoa parasites that infect a variety of vertebrate hosts. These parasites are capable of inducing life-threatening gastrointestinal disease in immunocompromised individuals. With the rising epidemiological evidence of the occurrence of <i>Cryptosporidium</i> infections in humans with digestive cancer, the tumorigenic potential of the parasite has been speculated. In this regard, <i>Cryptosporidium parvum</i> has been reported to induce digestive adenocarcinoma in a rodent model of chronic cryptosporidiosis. However, the processes by which the parasite could induce this carcinogenesis are still unknown. Therefore, the transcriptomes of <i>C. parvum</i> infected ileo-cecal regions of mice developing tumors were analyzed in the current study. For the first time, downregulation of the expression of α-defensin, an anti-microbial target of the parasite in response to <i>C. parvum</i> infection was observed in the transformed tissues. This phenomenon has been speculated to be the result of resistance of <i>C. parvum</i> to the host defense through the upregulated expression of interferon γ-stimulated genes. The inflammatory response generated as result of attenuated expression of anti-microbial peptides highlights the role of immune evasion in the <i>C. parvum</i>-induced tumorigenesis. The study has also succeeded in the characterization of the tumor microenvironment (TME) which is characterized by the presence of cancer associated fibroblasts, myeloid-derived suppressor cells, tumor-associated macrophages and extracellular matrix components. Identification of immune suppressor cells and accumulation of pro-inflammatory mediators speculates that chronic inflammation induced by persistent <i>C. parvum</i> infection assists in development of an immunosuppressive tumor microenvironment.