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Intestinal tissues (duodenum) from wild-type (BALB/c) and MIF deficient mice were compared in the steady state and at two different time points (day 3 and day 7) following infection with the gastrointestinal helminth parasite Heligmosomoides polygyrus

ABSTRACT: We have found that macrophage migration inhibitory factor (MIF) is essential for the development of effective immunity to the intestinal helminth Heligmosomoides polygyrus, even following vaccination which induces sterile immunity in wild-type mice. In the context of a Type 2 infection, MIF plays a critical role in polarizing macrophages into the protective alternatively-activated phenotype, and that STAT3 signaling may make a previously unrecognized contribution to immunity to helminths.

ORGANISM(S): Mus musculus

PROVIDER: GSE139008 | GEO | 2019/10/18

REPOSITORIES: GEO

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Duodenal tissues and mesenteric lymph nodes from wild-type (BALB/c) and MIF deficient mice were compared in the steady state and at day 5 following infection with the gastrointestinal helminth parasite Heligmosomoides polygyrus

Project description:We have found that macrophage migration inhibitory factor (MIF) is essential for the development of effective immunity to the intestinal helminth Heligmosomoides polygyrus, even following vaccination which induces sterile immunity in wild-type mice. In the context of a Type 2 infection, MIF plays a critical role in polarizing macrophages into the protective alternatively-activated phenotype, and that STAT3 signaling may make a previously unrecognized contribution to immunity to helminths.

2019-10-18 | GSE139007 | GEO

Heligmosomoides polygyrus

Project description:Heligmosomoides polygyrus overview

| PRJNA301368 | ENA

Gene expression analysis of ex-Foxp3 Th2 cells during Heligmosomoides polygyrus infection

Project description:Gene expression of Treg cells that have lost Foxp3 expression and acquired Il4 expression following adoptive transfer into T-cell deficient mice (HpTR-IL-4gfp+), cmpared to conventional Treg cells isolated from H. polygyrus-infected wild-type mice (HpTR) and Th2 cells generated from naïve T cells following adoptive transfer into H. polygyrus-infected T-cell deficient mice (nT-IL-4gfp+). Immunity to intestinal helminth infections requires the rapid activation of T helper 2 (Th2) cells. However, simultaneous expansion of regulatory CD4+Foxp3+ T (Treg) cells impedes protective responses, resulting in chronic infections. The ratio between regulatory and effector T cells can therefore determine the outcome of infection. The re-differentiation of Treg into T helper (Th) cells has been identified in hyper-inflammatory diseases. In this study, we asked whether ex-Treg Th2 cells develop and contribute to type 2 immunity. Using multi-gene reporter and fate-reporter systems we demonstrate that a significant proportion of Th2 cells derive from Foxp3+ cells following Heligmosomoides polygyrus infection and airway allergy. Ex-Foxp3 Th2 cells exhibit characteristic Th2 effector functions and provide immunity to H. polygyrus. Through selective deletion of Il4ra on Foxp3+ cells, we further demonstrate IL-4 is required for the development of ex-Foxp3 Th2 cells. Collectively, our findings indicate that converting Treg cells into Th2 cells could concomitantly enhance Th2 cells and limit Treg-mediated suppression.

2017-05-04 | GSE98518 | GEO

Genome sequencing of Heligmosomoides polygyrus bakeri

Project description:Genome sequencing of Heligmosomoides polygyrus bakeri

| PRJEB15396 | ENA

Heligmosomoides polygyrus

Project description:Exosomes secreted by a nematode parasite transfer small RNAs to mammalian cells and regulate genes of the innate immune system [Heligmosomoides polygyrus]

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RNAseq of murine small intestinal organoid cultures treated with Type 1 (IFNg) or Type 2 (IL4+IL13) cytokines in the presence or absence of excretory/secretory (ES) products of the helminth parasite Heligmosomoides polygyrus

Project description:Heligmosomoides polygyrus is a natural intestinal parasite of mice which exerts wide ranging modulatory effects on the immune system. This experiment was designed to investigate its abillity to modify intestinal epithelial cells, which form part of its natural niche. We tested gene expression in vitro, in differentiating organoids of small intestinal origin, exposed to cytokines and the released products of the parasite, termed HpES.

2021-11-12 | E-MTAB-11118 | biostudies-arrayexpress

Heligmosomoides polygyrus bakeri

Project description:Heligmosomoides bakeri overview

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The production of Excretory-Secretory molecules from Heligmosomoides polygyrus bakeri fourth stage larvae varies between mixed and single sex cultures.

Project description:In this study, the composition of ES of male and female L4 stage Heligmosomoides polygyrus bakeri in the presence (cultured together) or absence (cultured alone) of the opposite sex was examined using mass spectrometry.

2021-09-10 | PXD023759 | Pride

Impact of Heligmosomoides polygyrus infection on microbiota

Project description:Investigating the impact of Heligmosomoides polygyrus infection on the intestinal bacterial community in mouse.

| PRJEB10642 | ENA

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

2022-07-14 | GSE199226 | GEO

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