Expression data from mouse precision cut lung slices (PCLS) after human rhinovirus (RV) infection and after treatment with bronchobini (BRO).
Ontology highlight
ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE126832 | GEO | 2019/06/10
REPOSITORIES: GEO
Similar Datasets
Project description:Expression data from mouse precision cut lung slices (PCLS) after human rhinovirus (RV) infection and after treatment with bronchobini (BRO).
| PRJNA523417 | ENA
Project description:BackgroundAntiviral drugs such as rupintrivir may have an immune-modulatory effect in experimentally induced allergic asthma with subsequent RV infection. We infected lung slices of house-dust mite (HDM)-sensitized asthmatic mice ex vivo with human rhinovirus (RV) and investigated the effect of the antiviral drug rupintrivir on RV-induced cytokine response in lung tissue of HDM-sensitized mice ex vivo.MethodsMice were sensitized with HDM. Precision-cut lung slices (PCLS) were prepared from HDM-sensitized or non-sensitized mice. Lung slices were infected ex vivo with RV or RV together with rupintrivir. Modulation of immune responses was evaluated by cytokine secretion 48 h post infection.ResultsIn vivo HDM sensitization resulted in a TH-2/TH-17-dominated cytokine response that persisted in PCLS ex vivo. RV infection of PCLS from non-sensitized mice resulted in the induction of an antiviral and pro-inflammatory immune response, as indicated by the secretion of IFN-α, IFN-β, IFN-γ, TNF-α, MCP-1, IP-10, IL-10, and IL-17A. In contrast, PCLS from HDM-sensitized mice showed an attenuated antiviral response, but exaggerated IL-4, IL-6, and IL-10 secretion upon infection. Rupintrivir inhibited exaggerated pro-inflammatory cytokine IL-6 and TH-2 cytokine IL-4 in HDM-sensitized mice.ConclusionsIn summary, this study demonstrates that treatment with rupintrivir influences virus-induced IL-4 and IL-6 cytokine release under experimental conditions ex vivo.
| S-EPMC6805592 | biostudies-literature
Project description:Transcriptome analysis revealed miRNA profiles from PCLS of tumor-free tissue comparable to normal lung tissue Suitability of human PCLS as a model for lung-specific miRNA investigations by RTqPCR and microarray analyses
2021-06-22 | GSE167705 | GEO
Project description:BackgroundMonitoring cellular processes across different levels of complexity, from the cellular to the tissue scale, is important for understanding tissue structure and function. However, it is challenging to monitor and estimate these structural and dynamic interactions within three-dimensional (3D) tissue models.ObjectiveThe aim of this study was to design a method for imaging, tracking, and quantifying 3D changes in cell morphology (shape and size) within liver tissue, specifically a precision-cut liver slice (PCLS). A PCLS is a 3D model of the liver that allows the study of the structure and function of liver cells in their native microenvironment.MethodsHere, we present a method for imaging liver tissue during anisosmotic exposure in a multispectral four-dimensional manner. Three metrics of tissue morphology were measured to quantify the effects of osmotic stress on liver tissue. We estimated the changes in the volume of whole precision cut liver slices, quantified the changes in nuclei position, and calculated the changes in volumetric responses of tissue-embedded cells.ResultsDuring equilibration with cell-membrane-permeating and non-permeating solutes, the whole tissue experiences shrinkage and expansion. As nuclei showed a change in position and directional displacement under osmotic stress, we demonstrate that nuclei could be used as a probe to measure local osmotic and mechanical stress. Moreover, we demonstrate that cells change their volume within tissue slices as a result of osmotic perturbation and that this change in volume is dependent on the position of the cell within the tissue and the duration of the exposure.ConclusionThe results of this study have implications for a better understanding of multiscale transport, mechanobiology, and triggered biological responses within complex biological structures.
| S-EPMC10903333 | biostudies-literature
Project description:Members of rhinovirus C (RV-C) species are more likely to cause wheezing illnesses and asthma exacerbations compared to other rhinoviruses. The cellular receptor for these viruses was heretofore unknown. We measured gene expression (Human Gene 1.0 ST Array, Affymetrix) in two series of experiments involving cells that were either susceptible or not susceptible to RV-C infection. In one experimental series, susceptible cells included whole sinus mucosal tissue specimens (n = 5), epithelial cell suspension from sinus tissue, and nasal epithelium obtained via brushing, while non-susceptible cells included monolayers of primary undifferentiated epithelial cells and transformed cell lines (n = 5). In a second experimental series, we compared three pairs of undifferentiated and fully differentiated (ALI) sinus epithelial cell cultures. We identified a total of 12 genes upregulated in RV-C susceptible cells (represented by 14 probe sets) encoding proteins localized to plasma membrane, and/or with predicted or functionally demonstrated receptor activity, including members of the Human MHC class II, stomatin, guanine nucleotide-binding, type I cytokine and atypical chemokine receptor and cadherin protein families.
2014-11-01 | GSE61396 | GEO
Project description:We establish a mouse model of HCoV-NL63 and compare outcomes with a model of rhinovirus (RV)-A1B. Transgenic mice expressing human ACE2 were infected intranasally with sham LLC-MK2 cell lysate, 100,000 TCID50 units HCoV-NL63, or 1,000,000 PFU RV-A1B. Lungs were assessed for host gene expression by next generation sequencing. RNAseq showed increases in IFN-α, IFN-β, IFN-λ and many IFN-stimulated genes (ISGs) in NL63-infected mice. In addition to ISGs, RV-A1B induced expression of IFN-γ, IL-1β, NLRP3, TLR2 and C-X-C chemokines. We established a mouse model of HCoV-NL63 replicative infection characterized by expression of ISGs but fewer pro-inflammatory genes compared to RV-A1B.
2024-08-25 | GSE254967 | GEO
Project description:ObjectiveHuman precision cut lung slices (PCLS) are widely used as an ex vivo model system for drug discovery and development of new therapies. PCLS reflect the functional heterogeneity of lung tissue and possess relevant lung cell types. We thus determined the use of PCLS in studying non-coding RNAs notably miRNAs, which are important gene regulatory molecules. Since miRNAs play key role as mediators of respiratory diseases, they can serve as valuable prognostic or diagnostic biomarkers, and in therapeutic interventions, of lung diseases. A technical limitation though is the vast amount of agarose in PCLS which impedes (mi)RNA extraction by standard procedures. Here we modified our recently published protocol for RNA isolation from PCLS to enable miRNA readouts.ResultsThe modified method relies on the separation of lysis and precipitation steps, and a clean-up procedure with specific magnetic beads. We obtained successfully quality miRNA amenable for downstream applications such as RTqPCR and whole transcriptome miRNA analysis. Comparison of miRNA profiles in PCLS with published data from human lung, identified all important miRNAs regulated in IPF, COPD, asthma or lung cancer. Therefore, this shows suitability of the method for analyzing miRNA targets and biomarkers in the valuable human PCLS model.
| S-EPMC8252208 | biostudies-literature
Project description:Members of rhinovirus C (RV-C) species are more likely to cause wheezing illnesses and asthma exacerbations compared to other rhinoviruses. The cellular receptor for these viruses was heretofore unknown. We measured gene expression (Human Gene 1.0 ST Array, Affymetrix) in two series of experiments involving cells that were either susceptible or not susceptible to RV-C infection. In one experimental series, susceptible cells included whole sinus mucosal tissue specimens (n = 5), epithelial cell suspension from sinus tissue, and nasal epithelium obtained via brushing, while non-susceptible cells included monolayers of primary undifferentiated epithelial cells and transformed cell lines (n = 5). In a second experimental series, we compared three pairs of undifferentiated and fully differentiated (ALI) sinus epithelial cell cultures. We identified a total of 12 genes upregulated in RV-C susceptible cells (represented by 14 probe sets) encoding proteins localized to plasma membrane, and/or with predicted or functionally demonstrated receptor activity, including members of the Human MHC class II, stomatin, guanine nucleotide-binding, type I cytokine and atypical chemokine receptor and cadherin protein families. Sinus and bronchial epithelial tissue samples were obtained from residual surgical specimens. Primary airway epithelial cells were cultured submerged (undifferentiated monolayers) or at air-liquid interface (fully-differentiated). Established cell lines (HeLa, NCI-H358 and WisL) were cultured submerged. Epithelial tissue samples were placed in RNAlater solution (Life Technologies) to stabilize and protect cellular RNA; cultured cells were lysed directly and total RNAs were isolated using TRIzol reagent (Life Technologies). Gene expression was analyzed using the Human Genome 1.0 ST GeneChip arrays (Affymetrix, Santa Clara, CA).
2014-11-01 | E-GEOD-61396 | biostudies-arrayexpress
Project description:Respiratory infections caused by mycoplasma species in ruminants lead to considerable economic losses. Two important ruminant pathogens are Mycoplasma mycoides subsp. Mycoides (Mmm), the aetiological agent of contagious bovine pleuropneumonia and Mycoplasma mycoides subsp. capri (Mmc), which causes pneumonia, mastitis, arthritis, keratitis, and septicemia in goats. We established precision cut lung slices (PCLS) infection model for Mmm and Mmc to study host-pathogen interactions. We monitored infection over time using immunohistological analysis and electron microscopy. Moreover, infection burden was monitored by plating and quantitative real-time PCR. Results were compared with lungs from experimentally infected goats and cattle. Lungs from healthy goats and cattle were also included as controls. PCLS remained viable for up to two weeks. Both subspecies adhered to ciliated cells. However, the titer of Mmm in caprine PCLS decreased over time, indicating species specificity of Mmm. Mmc showed higher tropism to sub-bronchiolar tissue in caprine PCLS, which increased in a time-dependent manner. Moreover, Mmc was abundantly observed on pulmonary endothelial cells, indicating partially, how it causes systemic disease. Tissue destruction upon prolonged infection of slices was comparable to the in vivo samples. Therefore, PCLS represents a novel ex vivo model to study host-pathogen interaction in livestock mycoplasma.
| S-EPMC6631151 | biostudies-literature
Project description:Introduction: Viral respiratory infections cause considerable morbidity and economic loss. While rhinoviruses (RV) typically cause little more than the common cold, they can produce severe infections and disease exacerbations in susceptible individuals, including those with chronic lung diseases. Variations in the regulation of key antiviral cytokines, particularly type I interferon (IFN-α and IFN-b), may contribute to RV susceptibility, but are not well understood. Method: Whole genome transcription patterns were assessed in samples from 74 individuals demonstrating high or low IFN-α production following RV stimulation in vitro. Results: In unstimulated samples (baseline) the high IFN-α producer group showed higher expression of genes associated with plasmacytoid dendritic cells, the complement system, B-cell chemokines, immune regulation, macrophages, and vitamin D activation and lower expression of genes linked to haemoglobin and haem biosynthesis, wound healing, stress response and pro-inflammatory genes than the low IFN-α producer group. After RV stimulation, the high IFN-α producer group showed more intense upregulation of diverse immune function genes including IFNs and greater downregulation of genes linked to structural and extra-cellular matrix functions than the low IFN-α producer group. Patterns of antibacterial gene expression varied between groups. Healthy people and those with asthma generally showed similar gene expression patterns. These findings highlight multiple biological pathways whose expression patterns differ substantially between high and low IFN-α producers. These differences likely contribute to variations in anti-RV immunity and immunopathology between individuals.
2021-07-31 | GSE166292 | GEO