Abstract
Echinostoma caproni is an intestinal trematode that has been extensively used as an experimental model to investigate the factors determining the resistance to intestinal helminths or the development of chronic infections. ICR mice are permissive hosts for E. caproni in which chronic infections are developed, concomitantly with local Th1 responses, elevated levels of local IFN-γ, inflammation and antibody responses. However, mice develop partial resistance to homologous challenge infections after cure of a primary infection, which converts this subject into an adequate model for the study of the mechanisms generating resistance against intestinal helminths. The purpose of the present study was to compare the immune response induced in primary and secondary infections to elucidate the factors determining the different outcome of the infection in each type of infection. The results obtained indicate that susceptibility is determined by the lack of IL-25 expression in response to primary infection. In contrast, infection in an environment with elevated levels of IL-25, as occurs in challenge infection, results in a Th2 phenotype impairing parasite survival. This was confirmed by treatment of naïve mice with exogenous IL-25 and subsequent infection. Changes induced in goblet cell populations and mucin glycosylation could be implicated in resistance to infection.
Highlights
Intestinal helminth infections are among the most prevalent infections and it is estimated that more than 1.5 billion people are currently infected with one or more species of intestinal helminth mainly in Asia, Africa and Latin-America[1,2]
54% of mice belonging to the reinfected group became infected after secondary exposure to E. caproni metacercariae
Mice treated with rIL-25 were refractory to primary infection with 50 metacercariae of E. caproni and all the animals were negative at 3, 7 and 14 days post-primary infection
Summary
Intestinal helminth infections are among the most prevalent infections and it is estimated that more than 1.5 billion people are currently infected with one or more species of intestinal helminth mainly in Asia, Africa and Latin-America[1,2]. The resistance to E. caproni infection in hosts of low compatibility is associated with the development of a local Th2/Th17 phenotype and changes in tissue structure are not observed[17,18] Because of these characteristics, the E. caproni-rodent model is extensively used to elucidate several aspects of the host-parasite relationships in intestinal infections, such as the induction of distinct effector mechanisms and their effectiveness in parasite clearance. Mice are permissive host for E. caproni[14,19], a recent study showed that primary infection in ICR mice induces acquired immunity against subsequent homologous infection which is manifested in reduced infection rate, worm recovery and growth[20] This makes the E. caproni/ICR mouse system an excellent model for the study of the mechanisms generating acquired immunity against intestinal helminths. We have analyzed other immune mechanisms induced by primary response that have been associated with resistance against intestinal helminth infections
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