Interleukin-25 Induces Resistance Against Intestinal Trematodes

Muñoz-Antolí, Carla; Cortés, Alba; Santano, Rebeca; Sotillo, Javier; Esteban, J. Guillermo; Toledo, Rafael

doi:10.1038/srep34142

Cited by 23 publications

(43 citation statements)

References 51 publications

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“…91 The advent of mucin-gene knockout mice positions the field to unequivocally test the role of mucus in the expulsion of a range of parasitic helminths. The goblet cell/mucus response can be driven by the helminthevoked TH2 response, principally IL-4 and IL-13 92,93 and IL-25 94 ( Fig. 3) and potentially by contact with the worms or their E/S products: the latter needs to be explored on a species-by-species basis.…”

Section: Helminth and Host-derived Factors Impact On Intestinal Barrimentioning

confidence: 99%

Helminths and intestinal barrier function

2017

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Approximately one-sixth of the worlds' population is infected with helminths and this class of parasite takes a major toll on domestic livestock. The majority of species of parasitic helminth that infect mammals live in the gut (the only niche for tapeworms) where they contact the hosts' epithelial cells. Here, the helminth-intestinal epithelial interface is reviewed in terms of the impact on, and regulation of epithelial barrier function, both intrinsic (epithelial permeability) and extrinsic (mucin, bacterial peptides, commensal bacteria) elements of the barrier. The data available on direct effects of helminths on epithelial permeability are scant, fragmentary and pales in comparison with knowledge of mobilization of immune reactions and effector cells in response to helminth parasites and how these impact intestinal barrier function. The interaction of helminth-host and helminthhost-bacteria is an important determinant of gut form and function and precisely defining these interactions will radically alter our understanding of normal gut physiology and pathophysiological reactions, revealing new approaches to infection with parasitic helminths, bacterial pathogens and idiopathic auto-inflammatory disease.

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Section: Helminth and Host-derived Factors Impact On Intestinal Barrimentioning

confidence: 99%

Helminths and intestinal barrier function

2017

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“…Recent studies of our group showed that partial resistance against E. caproni secondary infections is developed after chemotherapeutic cure of a primary infection and innately produced IL-25 is crucial to determine the resistance. Susceptibility to primary infections was associated with low levels of intestinal IL-25 expression, whilst deworming via administration of praziquantel was accompanied by a steady increase in IL-25 expression that prevented the establishment of secondary infections [14][15]. However, it is not well defined if the participation of IL-25 in resistance to infection.…”

Section: Discussionmentioning

confidence: 99%

“…Previous studies of our group have shown that IL-25 is essential for the resistance to E. caproni infections and the susceptibility of mice relies on the inability of this host species to produce IL-25 in response to infection [14][15]. Susceptibility of mice to primary E. caproni infection was associated with low levels of intestinal IL-25 expression, whilst deworming via administration of praziquantel (pzq) was accompanied by a steady increase in IL-25 expression and, in turn, by the onset of a Th2type response that prevented the establishment of secondary infections [14][15]. Although these facts, little is known about the mechanism by which IL-25 generates resistance against intestinal helminths.…”

Section: Introductionmentioning

confidence: 99%

Ileal proteomic changes associated with IL-25-mediated resistance against intestinal trematode infections

Álvarez-Izquierdo

Esteban

Muñoz-Antolí

et al. 2020

Preprint

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Abstract Background: Echinostoma caproni (Trematoda: Echinostomatidae) is an intestinal trematode, which has been widely employed to investigate the factors determining the rejection of intestinal helminths. In this sense, several studies have shown that IL-25 is essential for the development of resistance against E. caproni in mice. In fact, treatment of mice with recombinant IL-25 generates resistance against primary E. caproni infection. However, the mechanisms by which IL-25 induces resistance remain unknown.Methods: To study the mechanisms responsible for resistance elicited by IL-25, we analyze the ileal proteomic changes induced by IL-25 in mice and their potential role in resistance. To this purpose, we compare the protein expression profiles in the ileum of four experimental groups of mice: naïve controls; E. caproni-infected mice; rIL-25-treated mice; and rIL-25-treated mice exposed to E. caproni metacercariae.Results: Quantitative comparison by 2D-DIGE showed significant changes in a total of 41 spots. Forty of those spots validated protein spots were were identified by mass spectrometry corresponding to 24 proteins.Conclusions: The analysis of differentially expressed proteins indicates that maintenance of the intestinal epithelial homeostasis and the regulation of proliferation and cell death are the most affected processes that appears to be related to the resistance to infection. These results provide new insights into the proteins involved in the regulation of tissue homeostasis after intestinal infection and its transcendence in resistance.

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“…Recent studies of our group showed that partial resistance against E. caproni secondary infections is developed after chemotherapeutic cure of a primary infection and innately produced IL-25 is crucial to determine the resistance. Susceptibility to primary infections was associated with low levels of intestinal IL-25 expression, whilst deworming via administration of praziquantel (pzq) was accompanied by a steady increase in IL-25 expression and, in turn, by the onset of a Th2-type response that prevented the establishment of secondary infections [26][27].…”

Section: Author's Summary Introductionmentioning

confidence: 99%

“…Herein, we have shown that mice also are unable to produce IL-25 in a secondary challenge infection.Despite this fact, secondary E. caproni infection at 2 wppt induced a Th2 response. This was attributed to the presence of elevated levels of IL-25 produced after the cure of the primary infection[26]. However, blocking of the IL-25 innately produced after healing of the primary infection gave rise to a type 2 response as a consequence of the secondary infection showing that IL-25 was not related to the biasing of the immune response.…”

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confidence: 99%

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

Álvarez-Izquierdo

Pérez-Crespo

Esteban

et al. 2020

Preprint

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Interleukin-25 (IL-25) plays a major role in resistance against intestinal helminth infections as initiator of protective Th2 responses. However, recent studies have challenged the contribution of this cytokine in both the polarization of the response towards a Th2 phenotype and the parasite rejection. We have used the experimental model Echinostoma caproni-ICR mice to investigate the participation of this cytokine in resistance to intestinal helminths. ICR mice are characterized by their inability to respond with IL-25 production in primary infections with E. caproni, causing susceptibility associated with a Th1 response. However, mice are refractory to infection in presence of IL-25 in relation to a type 2 phenotype. Herein, we show that dynamics of resident microbiota appears to be crucial in IL-25 production. Moreover, IL-25 seems to play a pivotal role in the polarization to Th2 in primary responses, but also appears to participate in the generation of memory mechanisms making unnecessary the participation of IL-25 in memory responses for the development of Th2 milieu. However, resistance to E. caproni infection does not depend on the generation of a Th2 phenotype, but exclusively depends on the presence of IL-25, operating autonomously from the type 2 response in the generation of resistance.

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Interleukin-25 Induces Resistance Against Intestinal Trematodes

Cited by 23 publications

References 51 publications

Helminths and intestinal barrier function

Helminths and intestinal barrier function

Ileal proteomic changes associated with IL-25-mediated resistance against intestinal trematode infections

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

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