Interleukin-25-mediated resistance against intestinal trematodes does not depend on the generation of Th2 responses
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RESEARCH
Interleukin‑25‑mediated resistance against intestinal trematodes does not depend on the generation of Th2 responses María Álvarez‑Izquierdo, Miguel Pérez‑Crespo, J. Guillermo Esteban, Carla Muñoz‑Antoli and Rafael Toledo*
Abstract Background: The cytokine interleukin-25 (IL-25) is recognized as the most relevant initiator of protective T helper 2 (Th2) responses in intestinal helminth infections. This cytokine induces resistance against several species of intestinal helminths, including the trematode Echinostoma caproni. E. caproni has been extensively used as an experimental model to study the factors determining resistance to intestinal infections. In the study reported here, we assessed the role of IL-25 in the generation of resistance in mice infected with E. caproni. Methods: The factors that determine the production of IL-25 in mice experimentally infected with E. caproni were determined, as were the consequences of IL-25 production in terms of polarization of the immune response and resistance to infection. Results: Our results show that the role of IL-25 in the polarization of the immune response differs between the primary and secondary immune responses. IL-25 is required for the development of a Th2 phenotype in primary E. caproni infections, but it can also promote the differentiation to Th2 memory cell subsets that enhance type-2 immunity in memory responses. However, the development of Th2 responses does not induce resistance to infec‑ tion. The Th2 phenotype does not elicit resistance, and IL-25 is responsible for the resistance regardless of its type-2 cytokine activity and activation of signal transducer and activator of transcription (STAT6). Alternative activation of macrophages induced by IL-25 can be implicated in the resistance to infection. Conclusions: In contrast to primary infection, secondary infection elicits a type-2 immune response even in the absence of IL-25 expression. Despite the development of a type-2 response, mice are susceptible to secondary infec‑ tion associated with the lack of IL-25. Resistance to infection is due to the production of IL-25, which acts autono‑ mously from Th2 response in terms of parasite clearance. Keywords: Interleuquin-25, Intestinal helminth, Th2, Resistance, Trematoda, Echinostoma caproni Background Intestinal helminth infections are common in humans and animals, especially in developing regions of Africa, Asia and the Americas [1–3]. In humans, these parasitic infections generate substantial morbidity and produce *Correspondence: [email protected] Área de Parasitología, Departamento de Farmacia y Tecnología Farmacéutica y Parasitología, Facultad de Farmacia, Universitat de València, Avda. Vicent Andrés Estellés s/n, Burjassot, 46100 Valencia, Spain
relevant physical and mental disorders that are often aggravated in the presence of serious economic problems [2]. In addition, infections by intestinal helminths compromise the health and productivity of livestock worldwide [3]. At the present time, the impac
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