0000000001311931
AUTHOR
Miguel Pérez-crespo
Additional file 1 of Interleukin-25-mediated resistance against intestinal trematodes does not depend on the generation of Th2 responses
Additional file 1: Table S1. Applied Biosystems Inventoried assays used in the present work.
Interleukin-25-mediated resistance against intestinal trematodes does not depend on the generation of Th2 responses
AbstractInterleukin-25 (IL-25) is recognized as the most relevant initiator of protective Th2 responses in intestinal helminth infections. It is well known that IL-25 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 the resistance to intestinal infections. Herein, we assessed the role of IL-25 in the generation of resistance in mice to E. caproni infections. ICR mice are permissive hosts for E. caproni in which chronic infections are developed in relation to the lack of IL-25 production in response to primary infection and the consequ…
Additional file 5 of Interleukin-25-mediated resistance against intestinal trematodes does not depend on the generation of Th2 responses
Additional file 5: Fig. S4. Treatment of IL-25-treated-mice with mα-IL-4Rα or rIL-13Rα2 reduces STAT6 activation. Indirect immunofluorescence with anti-STAT6 (red) and anti-STAT6P (red) on intestinal tissue of IL-25-treated-mice that were also treated with mα-IL-4Rα or rIL-13Rα2 at 2 weeks post-primary infection. Scale bar: 30 μm.
Additional file 4 of Interleukin-25-mediated resistance against intestinal trematodes does not depend on the generation of Th2 responses
Additional file 4: Fig. S3. Secondary E. caproni infection induces expansion of tuft cells and GATA3 + cells. (A) Schematic representation of the experimental protocol; (B) Counts of tuft cell populations and (C) GATA3 + cells 2 weeks after primary infection (2 wppi), 2 weeks after treatment with pzq (2 wppt) and 2 weeks after secondary infection with E. caproni (2 wpsi). Vertical bars represent the standard deviation. a: significant differences with respect to naïve mice controls; b: significant differences between groups (p
Additional file 2 of Interleukin-25-mediated resistance against intestinal trematodes does not depend on the generation of Th2 responses
Additional file 2: Fig. S1. Treatment of mice with rIL-4 or rIL-13 induces a Th2 response and RELM-β overexpression in response to primary Echinostoma caproni and infection but not resistance to infection. (A) expression of cytokine mRNA in the intestinal tissue of rIL-4-treated or rIL-13-treated mice at 2 weeks post-primary infection with E. caproni; (B) expression of RELM-β mRNA in the intestinal tissue (F) of naïve mice, non-infected rIL-4- or rIL-13-treated mice and infected rIL-4- or rIL-13-treated mice at 2 weeks post-primary infection. The relative quantities (RQ) of cytokine genes are shown after normalization with β-actin and standardization of the relative amount against day 0 sam…
Additional file 3 of Interleukin-25-mediated resistance against intestinal trematodes does not depend on the generation of Th2 responses
Additional file 3: Fig. S2. Immunohistochemical images showing changes in tuft cell populations (A) and GATA3+ cells (B) 2 weeks after primary infection (2 wppi), 2 weeks after treatment with praziquantel (2 wppt) and 2 weeks after secondary infection with E. caproni (2 wpsi). Scale bar: 10 μm.