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Stat6 dependent gene expression in lung and small intestine

ABSTRACT: Gene expression in the lung and intestine of wild-type and stat6 deficient mice on BALB/c background infected with the helminth parasite Nippostrongylus brasiliensis was compared by competitive hybridization to spotted 70-mer oligonucleotide arrays. Keywords: other

ORGANISM(S): Mus musculus

PROVIDER: GSE2717 | GEO | 2005/07/27

SECONDARY ACCESSION(S): PRJNA92329

REPOSITORIES: GEO

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Stat6 dependent gene expression in lung and small intestine

Project description:Gene expression in the lung and intestine of wild-type and stat6 deficient mice on BALB/c background infected with the helminth parasite Nippostrongylus brasiliensis was compared by competitive hybridization to spotted 70-mer oligonucleotide arrays.

2010-06-09 | E-GEOD-2717 | biostudies-arrayexpress

B cell-intrinsic STAT6 controls the germinal center response in type 2 immunity

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B cell-intrinsic STAT6 controls the germinal center response in type 2 immunity

Project description:By investigating the germinal center (GC) formation in STAT6ko/WT bone marrow-mixed chimera we found that GC formation in type 2 immune responses is dependent on B cell intrinsic expression of IL-4/IL-13-induced genes. We therefore used microarrays to find Stat6 dependent genes that are important for germinal center formation and/or organization after infection with the nematode Nippostrongylus brasiliensis (N. brasiliensis). Bone marrow of STAT6ko (CD45.2+) and WT (CD45.1+) were mixed and injected in lethaly irradiated WT (CD45.1+) mice. After 8 weeks, 5 Bone marrow-mixed chimera were infected with N. brasiliensis and draining lymph nodes were collected at day 14 after the infection and pooled. RNA was isolated from sort-purified CD45.1+ or CD45.2+ GC B cells (B220+CD38loGL-7hi).

2014-05-26 | E-GEOD-47679 | biostudies-arrayexpress

Human resistin alters lung mRNA expression from helminth-infected lungs.

Project description:Goal: To examine the effects of human resistin during helminth infection. Methodology: To examine the function of human resistin (hResistin), we utilized transgenic mice expressing the human resistin gene along with its entire regulatory region (hRetnTg+). Following infection with the helminth Nippostrongylus brasiliensis, whole lung RNA was sequenced in hRetnTg+ mice, control hRetnTg- and naïve mice. Conclusion: In hRetnTg+ mice, many genes involved in inflammation and the immune system, specifically toll-like receptor signaling and chemokines, are significantly upregulated, suggesting that human resistin promotes TLR signaling and inflammation during helminth infection. Examination of whole lung mRNA from Nippostrongylus brasiliensis-infected lungs at day 7 in mice expressing human resistin

2014-11-14 | E-GEOD-60537 | biostudies-arrayexpress

Transcription profiling of mouse infected with hookworm to investigate induced persistent changes to the immunological environment of the lung

Project description:Infection with Nippostrongylus brasiliensis results in persistent changes to the lung environment. Cytokine profiling reveals a sustained increase in both Th1 and Th2 transcripts. Cellular populations of macrophages display an alternative phenotype, with upregulation of YM1, Arg1, Mrc1 as well as Class II MHC. These alternatively activated alveolar macrophages (AAAMs) also increase drastically in number. Subsequent challenge with house dust mite (HDM) Dermatophagoides pteronyssinus shows a reduced allergic phenotype, with decreased fold changes in effector cell cytokines of both the Th1 and Th2 variety indicative of the new regulatory environment established in the lung by helminth infection. Histological examination of the lung environment reveals a significant decrease in eosinophila and reduced mucous production by bronchial epithelial cells. Experiment Overall Design: BALB/c mice were challenged with 500 infectious L3 stage Nippostrongylus brasiliensis larvae subcutaneously. Mice were allowed to resolve their infection, then were sensitized twice with 75 allergy units (AU) of HDM bound to 1mg of alum intraperitoneally. Two challenge doses of 50AU HDM in PBS were given intranasally one day apart, then lungs were harvested at 6, 24 and 72 hours post challenge. Mice were analyzed by histology, immunohistochemistry, real time RT-PCR and affymetrix gene array analysis using full genome chips.

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Human resistin alters lung mRNA expression from helminth-infected lungs.

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Project description:We used microarrays to find Stat6 dependent genes in control and IL-4 exposed bone marrow derived macrophages. Alternatively activated macrophages (AAM) accumulate in tissues during Th2-associated immune responses like helminth infections and allergic disorders. These cells possess potent inhibitory activity against T cells. The differentiation of AAM depends on IL-4/IL-13-mediated activation of the transcription factor Stat6. Stat6 is also required in AAM to induce several genes, such as YM1, FIZZ1 and Arginase1.

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STAT6-regulated genes in mouse B cells

Project description:The IL-4-induced and STAT6-dependent gene expression profile in mouse B cells was analyzed. Untouched B cells from 9 weeks old female Ly5.1-congenic wild-type and Ly5.2-congenic STAT6-deficient mice, both on BALB/c background, were isolated from the spleen and stimulated for 4 days in vitro with LPS and anti-CD40 in the presence or absence of IL-4.

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Epithelial-Cell-Derived Phospholipase A2 Group 1B Is an Endogenous Anthelmintic

Project description:Immunity to intestinal helminth infections has been well studied, but the mechanism of helminth killing prior to expulsion remains unclear. Here we identify epithelial-cell-derived phospholipase A2 group 1B (PLA2g1B) as a host-derived endogenous anthelmintic. PLA2g1B is elevated in resistant mice and is responsible for killing tissue-embedded larvae. Despite comparable activities of other essential type-2-dependent immune mechanisms, Pla2g1b-/- mice failed to expel the intestinal helminths Heligmosomoides polygyrus or Nippostrongylus brasiliensis. Expression of Pla2g1b by epithelial cells was dependent upon intestinal microbiota, adaptive immunity, and common-gamma chain-dependent signaling. Notably, Pla2g1b was downregulated in susceptible mice and inhibited by IL-4R-signaling in vitro, uncoupling parasite killing from expulsion mechanisms. Resistance was restored in Pla2g1b-/- mice by treating infective H. polygyrus L3 larvae with PLA2g1B, which reduced larval phospholipid abundance. These findings uncover epithelial-cell-derived Pla2g1b as an essential mediator of helminth killing, highlighting a previously overlooked mechanism of anti-helminth immunity.

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Transcription profiling of lungs from SCID and wild type mice infected with L3 stage infectious Nippostrongylus brasiliensis to examine the innate immune response to helminth infection in the lung.

Project description:The goal of this experiment was to examine the innate immune response to helminth infection in the lung. Hookworms (like many other helminths) use an obligate migration pathway through the lung. Their infection has been characterized in the gut in detail, but early immune responses in the lung have not been fully characterized. Experiment Overall Design: SCID mice were used to examine the innate immune response. SCID mice have no functional B or T cells but a fully functional innate immune system. SCID and WT mice were infected with 500 L3 stage infectious Nippostrongylus brasiliensis SC and their lungs were removed at days 2,3,4,8 and 12 post infection.

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