Concomitant immunity against superimposed homologous Echinostoma caproni infections in mice is mediated by interleuquin-25.

Abstract

BACKGROUND: The Institute of Cancer Research (ICR) mouse-Echinostoma caproni model is used to study mechanisms generating resistance against intestinal helminths due to the development chronic primary infections with Th1 responses, and partial resistance to secondary infections. OBJECTIVES: This study aimed to evaluate the generation of concomitant immunity against superimposed homologous E. caproni infection. METHODS: Changes in cytokine expression and macrophages markers as a consequence of primary infection, superimposed infection and superimposed infection in anti (α)-interleuquin(IL)-25-treated mice were investigated by real-time polymerase chain reaction (PCR). Translocation and phosphorylation of STAT6 were studied by indirect immunofluorescence (IIF) on intestinal tissue sections. The IIF technique was also used to label M1 and M2 macrophages to confirm the activation pathways. FINDINGS: Primary E. caproni infections elicit partial resistance against homologous superimposed infections. The animal groups displayed distinct patterns in the expression of cytokines, macrophages markers and IL-13Rα2 as well as STAT6 phosphorylation in a process mediated by IL-25. Resistance appears to rely on the ability of to induce IL-13Rα2 upregulation. MAIN CONCLUSIONS: The concomitant immunity is based the production of IL-25, rather than in the development of Th2 responses. Regarding the IL-25-dependent mechanisms responsible for concomitant immunity, the ability of IL-25 to induce IL-13Rα2 upregulation which serves to limit the production of other regulatory proteins such as Ym1 affecting the maintenance of mucosal homeostasis appears to be critical.