Transcription profiling of lung from mice challenged with cockroach antigen and treated with a drug, compound A
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ABSTRACT:
ORGANISM(S): Mus musculus
SUBMITTER: Narimene Lekmine
PROVIDER: E-TABM-499 | biostudies-arrayexpress |
REPOSITORIES: biostudies-arrayexpress
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Project description:These samples are part of a study in which we demonstrate that mast cells express the receptor CRTH2, which is the target for our antagonist compound compound A. We want to examine whether there are differences in RNA expression when the mast cells are treated with the ligands of CRTH2 - PGD2 and DK-PGD2 - compared to no treatment. Also, we want to see if pretreating the cells with compound A can block or change differences in RNA expression induced by either DK-PGD2 or PGD2. The study also looks at Ige loaded cells exposed to antigen and dexamethasone, and cells treated with BW868c - a a highly selective DP receptor antagonist.
2010-06-25 | E-TABM-498 | biostudies-arrayexpress
Project description:Rationale: Augmented smooth muscle contractility of the airways is one of the causes of airway hyperresponsiveness in asthmatics. However, the mechanism of the altered properties of airway smooth muscle cells is not well understood. Objectives: To identify differentially expressed genes (DEGs) related to the bronchial smooth muscle (BSM) hyper-contractility in a murine asthma model. Methods: The ovalbumin (OA)-sensitized mice were repeatedly challenged with aerosolized OA to induce asthmatic reaction. Transcriptomic profiles were generated by microarray analysis of BSMs from the OA-challenged and control animals, and KEGG (Kyoto Encyclopedia of Genes and Genomes) Pathway Analysis was applied. Measurements and Main Results: Tension study showed a BSM hyperresponsiveness to acetylcholine (ACh) in the OA-challenged mice. A total of 770 genes were differentially expressed between the OA-challenged and control animals. Pathway analysis showed a significant change in arachidonic acid (AA) metabolism pathway in BSMs of the OA-challenged mice. Validation of DEGs by quantitative RT-PCR showed a significant increase in PLA2 group 4c (Pla2g4c)/COX-2 (Ptgs2)/PGD2 synthase 2 (Hpgds) axis. PGD2 level in bronchoalveolar fluids of the OA-challenged mice was significantly increased. A 24-h incubation of BSMs with PGD2 caused a hyperresponsiveness to ACh in naive control mice. Conclusions: AA metabolism is shifted towards PGD2 production in BSMs of asthma. Increased PGD2 level in the airways might be a cause of the BSM hyperresponsiveness in asthma.
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Project description:Exposure to dogs in early infancy has been shown to reduce the risk of childhood allergic disease development and dog-ownership is associated with a distinct house dust microbial exposure. Here we demonstrate, using murine models, that exposure of mice toM-BM- dog-associated house dust protects against ovalbumin or cockroach allergen mediated airway pathology. Protected animals exhibited significant reductions in the total number of airway T cells, down-regulation of Th2-related airway responses as well as mucin secretion. Following house dust exposure, the cecal microbiome of protected animals was extensively restructured with significant enrichment of, amongst others, Lactobacillus johnsonii. Supplementation of wild type animals with L. johnsonii protected them against both airway allergen challenge or infection with respiratory syncytial virus. L. johnsonii mediated protection wasM-BM- associated with significant reductions in the total number and proportion of activated CD11c+/CD11b+ and CD11c+/CD8+ cells, as well as significantly reduced airway Th2 cytokine expression. Our results reveal that exposure to dog-associated household dust results in protection against airway allergen challenge and a distinct GI microbiome composition. Moreover the study identifies L. johnsonii as a pivotal species within the gastrointestinal tract capable of influencing adaptive immunity at remote mucosal surfaces in a manner that is protective against a variety of respiratory insults. The G2 PhyloChip microarray platform (commercially available from Second Genome, Inc.) was used to profile cecal gut bacteria from 29 mice: 7 controls, 5 gavaged with dust from homes with pets, 5 gavaged with dust from homes with no pets, 4 CRA-challenged, 4 gavaged with L. johnsonii, and 4 gavaged with L. johnsonii prior to CRA challenge. The PhyloChip was also used to profile 1 house dust sample collected from a home with dogs
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2013-12-20 | E-GEOD-52906 | biostudies-arrayexpress
Project description:Exposure to dogs in early infancy has been shown to reduce the risk of childhood allergic disease development and dog-ownership is associated with a distinct house dust microbial exposure. Here we demonstrate, using murine models, that exposure of mice toM-BM- dog-associated house dust protects against ovalbumin or cockroach allergen mediated airway pathology. Protected animals exhibited significant reductions in the total number of airway T cells, down-regulation of Th2-related airway responses as well as mucin secretion. Following house dust exposure, the cecal microbiome of protected animals was extensively restructured with significant enrichment of, amongst others, Lactobacillus johnsonii. Supplementation of wild type animals with L. johnsonii protected them against both airway allergen challenge or infection with respiratory syncytial virus. L. johnsonii mediated protection wasM-BM- associated with significant reductions in the total number and proportion of activated CD11c+/CD11b+ and CD11c+/CD8+ cells, as well as significantly reduced airway Th2 cytokine expression. Our results reveal that exposure to dog-associated household dust results in protection against airway allergen challenge and a distinct GI microbiome composition. Moreover the study identifies L. johnsonii as a pivotal species within the gastrointestinal tract capable of influencing adaptive immunity at remote mucosal surfaces in a manner that is protective against a variety of respiratory insults. The G2 PhyloChip microarray platform (commercially available from Second Genome, Inc.) was used to profile cecal gut bacteria from 29 mice: 7 controls, 5 gavaged with dust from homes with pets, 5 gavaged with dust from homes with no pets, 4 CRA-challenged, 4 gavaged with L. johnsonii, and 4 gavaged with L. johnsonii prior to CRA challenge. The PhyloChip was also used to profile 1 house dust sample collected from a home with dogs
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Project description:A highly specific and potent small molecule antagonist of CRTH2 (chemoattractant receptor) was used to investigate the role of this Prostaglandin D2 (PGD2) receptor in chronic models of cutaneous inflammation and the underlying immune response. These RNA samples are from mice that were in a chronic (50 day) model of atopic dermatitis. Each mouse had a section of back skin patched with a gauze, and the RNA was from the patched area of skin; the control mice had the gauze soaked in PBS, whereas all the other test mice had the gauze soaked in ovalbumin dissolved in PBS. The ovalbumin acts as an allergen and induces the experimental atopic dermatitis. The six groups of mice that received the OVA patch were treated in different ways:some received just the drug vehicle during the OVA patching, others received the test drug (compound A) at 3 different concentrations: 10 mg/kg 1 mg/kg and 0.1 mg/kg. Two other cohorts received positive control drugs: ramatroban and dexamethasone .Each different sample represents a different animal.
2009-06-25 | E-TABM-505 | biostudies-arrayexpress
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Project description:The role of CRTH2 (chemoattractant receptor) in a murine allergic contact inflammation model of human Atopic Dermatitis was investigated.This an acute model of atopic dermatitis in which a CRTH2 antagonist (compound A) and a positive control drug (dexamethasone, Dex) were evaluated. The experimental protocol was as follows:the mice first had their stomach area shaved, and either FITC (Fluorescein isothiocyanate) or the vehicle FITC is dissolved in (acetone:DBPTH) is applied to the skin on day 1 and day 2. The mouse generated an immune response to FITC and made specific antibodies. Six days later, the mouse was challenged, which consisted of putting FITC on the right ear and the vehicle w/o FITC (acetone:DBPTH) on the left ear. After 24 hrs. the thickness of each ear was measured, and to gauge the level of swelling/inflammation, the thickness of the left ear was compared to the FITC treated right ear. To assess the ability of the drug to block inflammation, the difference in R/L ear thickness were comparedfrom the mice that received FITC on the right ear, and drug vehicle (FITC/Vehicle group) to the group that received FITC on the right ear and either compound A (FITC/compound A) or dexamethasone (FITC/Dex). The control group only had vehicle (acetone:DBPTH) applied to the stomach area on days 1 & 2, and vehicle applied to both the right and left ears at the time of challenge. They also received the drug vehicle solution. The control animals did not mount a response to the vehicle (acetone:DBPTH) and did not have an increase in ear thickness compared to untreated animals.
2009-06-27 | E-TABM-522 | biostudies-arrayexpress
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