Interleukin-25-mediated resistance against intestinal trematodes does not depend on the generation of Th2 responses

Background: Interleukin-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. Echinostoma 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. Methods: To this purpose, we analyze the fatros that determine the production of IL-25 in mice experimentally infected with E. caproni and its consequences in the polarization of the immune response and the resistance to infection.Results: We have determined that the role of IL-25 in the polarization of the immune response differs between the primary and secondary response. IL-25 is required for the development of a Th2 phenotype in primary E. caproni infections but could also promote the differentiation to Th2 memory cell subsets that enhances type 2 responses in memory responses. However, development of Th2 responses does not induce resistance to infection. Th2 phenotype does not elicit resistance and IL-25 is responsible for the resistance regardless of the type 2 cytokine activity and STAT6 activation. Alternative activation of macrophages induced by IL-25 could be implicated in the resistance to infection. Conclusions: In contrast to primary infection, secondary infection elicits a type 2 response, even in the absence of IL-25 expression. Despite the development of a type 2 response, mice are susceptible to secondary infection in relation to the lack of IL-25. Resistance to infection is due to IL-25, which acts autonomously from Th2 response in the parasite clearance.

Interleukin-25-Mediated Resistance Against Intestinal Trematodes Does Not Depend on The Generation of Th2 Responses

Background: Interleukin-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. Echinostoma 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. Methods: To this purpose, we analyze the fatros that determine the production of IL-25 in mice experimentally infected with E. caproni and its consequences in the polarization of the immune response and the resistance to infection.Results: We have determined that the role of IL-25 in the polarization of the immune response differs between the primary and secondary response. IL-25 is required for the development of a Th2 phenotype in primary E. caproni infections but could also promote the differentiation to Th2 memory cell subsets that enhances type 2 responses in memory responses. However, development of Th2 responses does not induce resistance to infection. Th2 phenotype does not elicit resistance and IL-25 is responsible for the resistance regardless of the type 2 cytokine activity and STAT6 activation. Alternative activation of macrophages induced by IL-25 could be implicated in the resistance to infection. Conclusions: In contrast to primary infection, secondary infection elicits a type 2 response, even in the absence of IL-25 expression. Despite the development of a type 2 response, mice are susceptible to secondary infection in relation to the lack of IL-25. Resistance to infection is due to IL-25, which acts autonomously from Th2 response in the parasite clearance.

Effects of Echinostoma caproni miracidia dose on the amino acid contents of Biomphalaria glabrata as determined by high-performance thin-layer chromatography

The effects of 5, 20, and 40 miracidia dose exposures of Echinostoma caproni on the amino acid contents of Biomphalaria glabrata were studied using high performance thin-layer chromatography-densitometry. Amino acids were identified and quantified in whole bodies of exposed snails and in the uninfected matched controls at 2 and 4 weeks post-exposure. Using cellulose layers with the mobile phase 2-butanol-pyridine-glacial acetic acid-deionized water (39:34:10:26) and ninhydrin detection reagent [2% ninhydrin in acetone-n-butanol (1:1)], five amino acids were identified, i.e., leucine/isoleucine, valine, alanine, glycine, and ornithine, by hRF value comparison and color differentiation. Quantitatively, there was a marked elevation in the amounts of four of these five amino acids (isoleucine/leucine, valine, alanine, and ornithine) across dose levels at 4 weeks post-infection (P<0.05). Elevation of the amino acid content in the high dose snail group suggested that some changes occurred in the amino acid metabolism of the snails in that group as a function of miracidia dose.