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Helminth-induced reprogramming of the stem cell niche inhibits type 2 immunity [scRNA-seq]

ABSTRACT: Enteric helminths form intimate physical connections with the intestinal epithelium, yet their ability to directly alter epithelial stem cell fate has not been resolved. Here we demonstrate that infection of mice with the symbiotic parasite Heligmosomoides polygyrus bakeri (Hpb), reprograms the intestinal epithelium into a fetal-like state marked by the emergence of Clusterin-expressing revival stem cells (revSCs). Organoid-based studies using parasite-derived excretory/secretory products reveal that Hpb-mediated revSC generation occurs independent of host-derived immune signals and inhibits type 2 cytokine-driven differentiation of secretory epithelial lineages that promote their expulsion. Reciprocally, type 2 cytokine signals limit revSC differentiation and, consequently, Hpb fitness indicating that helminths compete with their host for control of the intestinal stem cell niche to promote continuation of their life cycle.

ORGANISM(S): Mus musculus

PROVIDER: GSE199226 | GEO | 2022/07/14

REPOSITORIES: GEO

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Helminth-induced reprogramming of the stem cell niche inhibits type 2 immunity [Bulk RNA-seq]

Project description:Enteric helminths form intimate physical connections with the intestinal epithelium, yet their ability to directly alter epithelial stem cell fate has not been resolved. Here we demonstrate that infection of mice with the symbiotic parasite Heligmosomoides polygyrus bakeri (Hpb), reprograms the intestinal epithelium into a fetal-like state marked by the emergence of Clusterin-expressing revival stem cells (revSCs). Organoid-based studies using parasite-derived excretory/secretory products reveal that Hpb-mediated revSC generation occurs independent of host-derived immune signals and inhibits type 2 cytokine-driven differentiation of secretory epithelial lineages that promote their expulsion. Reciprocally, type 2 cytokine signals limit revSC differentiation and, consequently, Hpb fitness indicating that helminths compete with their host for control of the intestinal stem cell niche to promote continuation of their life cycle.

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Project description:This data is part of a pre-publication release. For information on the proper use of pre-publication data shared by the Wellcome Trust Sanger Institute (including details of any publication moratoria), please see http://www.sanger.ac.uk/datasharing/ The human-infective whipworm Trichuris trichiura is estimated to infect up to a billion people and is responsible for considerable morbidity, especially in children of developing countries. The closely related species T. muris is a naturally occurring nematode parasite of mice that serves as a remarkably tractable model system for dissecting immune responses and host-parasite relationships. Such studies are of relevance beyond parasitology as helminths have arguably had a significant impact on the evolution of the mammalian immune system. Both Trichuris species reside in the caecum and colon of the host where they burrow their front end for feeding into the intestinal mucosa, thereby breaching the mucus barrier and allowing access of the microflora directly to the epithelium. The interplay of intestinal helminths, the bacterial microflora and the host immune system is currently a research focus in various laboratories (Bancroft et al 2012). This study will study the transcriptional responses of the intestinal mucosa (caecum) from infected and uninfected mice.

2013-05-07 | E-ERAD-181 | biostudies-arrayexpress

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Project description:The weekly turnover of the intestinal epithelium is driven by multipotent, Lgr5+, crypt base columnar cells (CBCs). In response to injury, however, Lgr5+ cells are lost but then re-emerge and are required for successful recovery. How these resurgent Lgr5+ stem cells arise is unclear. We transcriptionally profiled single cells from regenerating intestinal epithelia and identified a unique cell type we term the revival stem cell (rSC). rSCs are mutually exclusive to CBCs and are distinguished by elevated expression of cell survival and DNA repair genes. In homeostasis, rSCs are extremely rare, but nevertheless give rise to all the major cell types of the intestine including crypt-villus axes. After damage rSCs display a 20-fold, Yap-dependent, transient expansion, reconstitute the Lgr5+ CBC compartment and are required to regenerate a functional intestine. These studies define a unique stem cell phenotype that is mobilized by damage to reconstitute the intestinal epithelium.

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Single-Cell Transcriptomes of the Regenerating Intestine Reveal a Revival Stem Cell [part 2]

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Placental gene expression in intestinal nematode-infected and protein-deficient mice

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Gall&Pin2022 - ODE model of the intestinal epithelium

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