Abstract

Abstract Whereas a causal association between viral and bacterial infections with tumor development has been well established in animal and epidemiological studies, the impact of parasitic infections in cancer development is almost unknown. Evidences indicate that cancer can be triggered by chronic or deregulated inflammatory processes, such as colitis-associated colorectal cancer (CAC). Using a helminth infection model, we have analyzed the role of helminth-induced anti-inflammatory response in determining the outcome of CAC. Following Taenia crassiceps infection and development of CAC, mice displayed inhibited colonic inflammatory responses and reduced circulating and colonic CD11b+Ly6C+CCR2+ monocytes. Instead they increased the expression of IL-4 and alternatively activated macrophages (AAMs) markers at the colonic tissue. Strikingly, T. crassiceps-infected mice developed few tumors and reduced pathology. In contrast, uninfected mice mounted strong inflammatory responses, did not express AAMs markers, developed severe pathology and displayed multiple tumors. Thus, immunomodulatory activities induced by helminth infections may have a role in the resistance and progression of CAC.

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