Abstract
BackgroundSchistosomes are trematode worms that dwell in their definitive host’s blood vessels, where females lay eggs that need to be discharged into the environment with host excreta to maintain their life-cycle. Both worms and eggs require type 2 immunity for their maturation and excretion, respectively. However, the immune molecules that orchestrate such immunity remain unclear. Interleukin (IL)-33 is one of the epithelium-derived cytokines that induce type 2 immunity in tissues. The aim of this study was to determine the role of IL-33 in the maturation, reproduction and excretion of Schistosoma mansoni eggs, and in the maintenance of egg-induced pathology in the intestines of mice.MethodsThe morphology of S. mansoni worms and the number of eggs in intestinal tissues were studied at different time points post-infection in S. mansoni-infected IL-33-deficient (IL-33−/−) and wild-type (WT) mice. IL-5 and IL-13 production in the spleens and mesenteric lymph nodes were measured. Tissue histology was performed on the terminal ilea of both infected and non-infected mice.ResultsWorms from IL-33−/− and WT mice did not differ morphologically at 4 and 6 weeks post-infection (wpi). The number of eggs in intestinal tissues of IL-33−/− and WT mice differed only slightly. At 6 wpi, IL-33−/− mice presented impaired type 2 immunity in the intestines, characterized by a decreased production of IL-5 and IL-13 in mesenteric lymph nodes and fewer inflammatory infiltrates with fewer eosinophils in the ilea. There was no difference between IL-33−/− and WT mice in the levels of IL-25 and thymic stromal lymphopoietin (TSLP) in intestinal tissues.ConclusionsDespite its ability to initiate type 2 immunity in tissues, IL-33 alone seems dispensable for S. mansoni maturation and its absence may not affect much the accumulation of eggs in intestinal tissues. The transient impairment of type 2 immunity observed in the intestines, but not spleens, highlights the importance of IL-33 over IL-25 and TSLP in initiating, but not maintaining, locally-induced type 2 immunity in intestinal tissues during schistosome infection. Further studies are needed to decipher the role of each of these molecules in schistosomiasis and clarify the possible interactions that might exist between them.Graphical
Highlights
Schistosomes are trematode worms that dwell in their definitive host’s blood vessels, where females lay eggs that need to be discharged into the environment with host excreta to maintain their life-cycle
As IL-33 is known to induce and/or amplify Alternatively activated macrophage (M2) polarization of macrophages [27, 29,30,31] which are essential for the excretion of schistosome eggs [14, 15], we considered the possibility that in addition to contributing to the maturation of schistosome worms through the induction of type 2 immunity during prepatent schistosome infection, IL-33 may play a role in the accumulation of S. mansoni eggs in the intestinal tissues
Because IL-33 is known to induce type 2 immunity independently of IL-4 [38] and in light of the results of a recent study [26] which reported increased S. japonicum worm numbers after injection of exogenous IL-33 into infected mice, we decided to investigate whether IL-33 deficiency would compromise the maturation of S. mansoni worms by comparing the morphology and number of worm pairs between IL-33−/− and WT mice
Summary
Schistosomes are trematode worms that dwell in their definitive host’s blood vessels, where females lay eggs that need to be discharged into the environment with host excreta to maintain their life-cycle. About half of these eggs are washed into the liver by blood flow from the mesenteric veins; of the remainder, one-third to one-half succeed in reaching the intestinal lumen to be discharged into the environment with the host’s feces, while the remaining eggs are trapped in intestinal tissues where they die, either killed by the host’s immune system or of natural death [4, 5] Through their excretory–secretory products (ESP), such as the interleukin (IL)-4-inducing principle of S. mansoni eggs (IPSE/α1) [6, 7] and omega-1 (ω1) [8] from S. mansoni and their homologs from S. haematobium [9] and S. japonicum [10], tissue-trapped eggs elicit strong and vigorous type 2 cell-mediated immunity that induces perioval granuloma formation and leads to fibrosis [11, 12], pathological characteristics of a patent schistosome infection. In addition to being protective for and yet smiting the host with the pathology, granulomas in intestines play a beneficial role for the parasite, favoring the escape of eggs from the host through the intestinal wall [14, 15]
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