1,721,012 research outputs found
IL-33 induces an antiviral signature in mast cells but enhances their permissiveness for human rhinovirus infection
No full textData used in the generation of figures for the above titled manuscript published in the journal 'Viruses'</span
Generation of mast cells from murine stem cell progenitors
No full textMouse bone marrow-derived mast cells (mBMMCs) are an invaluable tool for the study of mast cell function as they represent a primary source of mature mast cells. They can be sourced from wild-type, knockout, and transgenic mice and are used to repopulate mast cell-deficient mice. This method describes the isolation of mast cell hematopoietic progenitors from the bone marrow of mouse femurs and their subsequent culture in an IL-3-rich culture medium. After 4 weeks in culture, mBMMCs are obtained in high number and are of high purity. Assessment of their granularity by toluidine staining and IgE receptor expression by flow cytometry is also described. These cells are a useful tool in the determination of in vitro and in vivo mast cell function in innate and adaptive immunity
Data supporting the publication "Human Milk Extracellular Vesicles Preserve Bronchial Epithelial Barrier Integrity and Reduce TLR3-Induced Inflammation".
No full textThis dataset supports the publication: Human Milk Extracellular Vesicles Preserve Bronchial Epithelial Barrier Integrity and Reduce TLR3-Induced Inflammation
https://doi.org/10.1002/jex2.54
by Nikita Karra, Martijn J. C. Van Herwijnen, Marca H. M. Wauben, Emily Jane Swindle, Hywel Morgan
in Journal of extracellular biology
Volume1, Issue9 September 2022 pages e54
The Data has two folders supporting the information used to create the Graphs for the Article and summary of experiments.
2022_Vesicle_Paper_Data_Analysis.pzfx
VesicleData.xlsx
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Dataset in support of the University of Southampton Doctoral thesis 'Role of IL-33 on human mast cell responses to rhinovirus infection in asthma'
No full textThis dataset contains:
MC RNASeq Count files
• Individual Count files for each sample, used for producing data for Chapter 5 of my thesis.
• 42 samples.
• 6 conditions = Control, UVRV Control (MOI 5), RV (MOI 5), Control + IL33 (10ng/ml), UVRV (MOI 5) + IL33 (10ng/ml), RV (MOI 5) + IL33 (10ng/ml), all at 6 hours. 7 replicates. 2 batches, n=1-3 and n=4-7, from 2 defrosted batches of LAD2 MCs. Counts were aligned to GRCh38.99 human reference genome.
• 'Counts_table_collated.txt' is a table of all of the individual count files put into one table.
• 'Counts_table_applied_batch_effect_combat_log2cpm.txt' is the collated table, where log2 was applied to counts and batch effect was accounted for using the combat package. This was the counts table used for all further bioinformatics analysis.
Thesis Chapter 6 Validation Figures Files
• 'Chapter_6_Results_PRISM_Graphs.pzfx' - All the figures for Chapter 6 with statistics.
Thesis Chapter 5 RNASeq Analysis Figures Files
• Images, PRISM files, and Excel data that corresponds to the figures used for Chapter 5.
• 'Counts Input for Heatmaps' contains tables used for inputting data into Morpheus to create the heatmaps.
• 'Counts_table_applied_batch_effect_combat_log2pcm.txt' is the Counts table used for all analysis. This is the collated counts in one table, applied log2, and corrected for batch effect using Combat.
• 'Counts_table_collated.txt' is the collated counts in one table, without any corrections.
CSVs of differentially expressed genes identified per comparison in Chapter 5 Results
• Differentially expressed genes (DEGs) were defined as genes that had a fold change of over 1.5 and a FDR-adjusted p value of less than 0.05.
• 'FC1.5_C.IL33vC.csv' contains list of 2,001 DEGs when comparing Control v Control+IL33
• 'FC1.5_RVvUV.csv' contains list of 135 DEGs when comparing UVRV v RV
• 'FC1.5_UV.IL33vUV.csv' contains list of 1938 DEGs when comparing UVRV v UVRV+IL33
• 'FC1.5_RV.IL33vUV.csv' contains list of 2564 DEGs when comparing UVRV v RV+IL33
• 'FC1.5_UVvC.csv' contains list of 0 DEGs when comparing Control v UVRV
Thesis Chapter 4 Optimisation Results Figures Files
• 'Figures for Chapter 4.pzfx' is the GraphPad PRISM file containing all figures produced for Chapter 4. Please note that figure numbers in this file does not correspond directly to Thesis figure numbers. Please see 'Information accompanying Figures for Chapter 4.docx'
• 'Accompanying statistics for Chapter 4 figures.pzfx' is the GraphPad PRISM file that contains all the statistics calculations for all the figures from 'Figures for Chapter 4.pzfx'. Please note that figure numbers in this file does not correspond directly to Thesis figure numbers. Please see 'Information accompanying Figures for Chapter 4.docx'
• 'Information accompanying Figures for Chapter 4.docx' is a table that details which figure number in the Thesis corresponds to the Figures and Statistics produced in the above PRISM files.
Thesis Chapter 3 BMMCs Analysis Figures Files
• 'Figures for Chapter 3 - 3-1 to 3-13.pptx' is a powerpoint of figures used in this chapter.
• 'Figures 3-4, A-B Tables - workbook for clustvis.xlsx' - contains data for Figures 3-4, alongside data input to create the heatmaps in clustvis for this chapter.
• 'DEG_WT.IgE.csv' - is the list of 772 differentially expressed genes when comparing WT unstimulated vs WT IgE/Ag.
• 'DEG_ST2KO.WT.csv' - is the list of 2 differentially expressed genes when comparing WT unstimulated vs ST2KO unstimulated.
• 'DEG_ST2KO.WT.IgE.csv' - is the list of 2 differentially expressed genes when comparing WT IgE/Ag vs ST2KO IgE/Ag.
• 'DEG_ST2KO.IgE.csv' - is the list of 782 differentially expressed genes when comparing ST2KO unstimulated vs ST2KO IgE/Ag.
• 'DEG_WT.IL33.csv' - is the list of 781 differentially expressed genes when comparing WT unstimulated vs WT IL33.
• 'DEG_ST2KO.IL33.csv' - is the list of 0 differentially expressed genes when comparing ST2KO unstimulated vs ST2KO IL33.</span
Drug delivery for traditional and emerging airway models
No full textRespiratory diseases such as asthma and COPD have no cures and few new treatments. These diseases have an immutable mortality rate and impact millions of individuals worldwide. Respiratory drug development is time-consuming and costly, owing to the inability of existing models to replicate the complexity of human disease (static cell cultures and animal models). The problem is intensified through the way in which drugs are delivered to these models, which is not always representative of the human microenvironment, where different drug delivery methods (impaction, sedimentation and diffusion) target different regions of the lungs. This review describes current models of the human airways together with the range of different aerosol drug delivery methods (commercially available and in development) alongside emerging Organ on Chip technologies
On chip label-free epithelial barrier function assay in artificial human asthmatic airway
No full textDataset for "Droplet fluidics for time- dependent analysis of barrier permeability in an epithelial barrier on chip system".
No full textDataset to support the publication of "Droplet fluidics for time- dependent analysis of barrier permeability in an epithelial barrier on chip system".
This dataset contains:
. CellData.zip - Zipped folder with data collected for 16HBE14o- experiments with Triton and dextran-FITC. Data includes both fluorescence and impedance spectroscopy.
. DropletData.opju - Project folder to be opened using Origin 2021 or latest. Collection of all data used in the paper, including COMSOL simulations, droplet size variation and cell data.
. FITC_8_Channel_Device.xlsx - Excel file with data collected during FITC apical-to-basolateral diffusion throug the microfluidic chip. To be opened with Excel compatible software.
. DropletSizeVariation.xlsx - Excel file with data collected for droplet size generation used to assess droplet size variation over 33 hours. To be opened with Excel compatible software.
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Artificial airways for the study of respiratory disease
No full textThis review will focus on human cell-based experimental models to study respiratory diseases, in particular models of the large airways relevant to asthma and chronic obstructive pulmonary disease. Such models have the advantage of incorporating cells that can be derived from disease-relevant tissue and so have retained important genetic and epigenetic features that contribute to the human disease. These models can be used for mechanistic studies, target identification and validation and toxicological testing. While many models have been developed to varying degrees of sophistication, the challenge remains to develop an integrated system that recapitulates the complex cell-cell and cell-matrix interactions that occur in vivo and to provide these with a 'circulation' to study the dynamics of immune and inflammatory cell influx and efflux
Integrating an aerosolised drug delivery device with conventional static cultures and a dynamic airway barrier microphysiological system
No full textDataset to support publication: Integrating an aerosolised drug delivery device with conventional static cultures and a dynamic airway barrier microphysiological system. to be published in the journal Microfluidics</span
Mast cells are permissive for rhinovirus replication: potential implications for asthma exacerbations
No full textBACKGROUND: Human rhinoviruses (HRVs) are a major trigger of asthma exacerbations, with the bronchial epithelium being the major site of HRV infection and replication. Mast cells (MCs) play a key role in asthma where their numbers are increased in the bronchial epithelium with increasing disease severity.OBJECTIVE: In view of the emerging role of MCs in innate immunity and increased localisation to the asthmatic bronchial epithelium, we investigated whether HRV infection of MCs generated innate immune responses which were protective against infection.METHODS: The LAD2 MC line or primary human cord blood-derived MCs (CBMCs) were infected with HRV or UV-irradiated HRV at increasing multiplicities of infection (MOI) without or with IFN-? or IFN-?. After 24 h, innate immune responses were assessed by RT-qPCR and IFN protein release by ELISA. Viral replication was determined by RT-qPCR and virion release by TCID50 assay.RESULTS: HRV infection of LAD2 MCs induced expression of IFN-?, IFN-? and IFN-stimulated genes. However, LAD2 MCs were permissive for HRV replication and release of infectious HRV particles. Similar findings were observed with CBMCs. Neutralisation of the type I IFN receptor had minimal effects on viral shedding suggesting that endogenous type I IFN signalling offered limited protection against HRV. However, augmentation of these responses by exogenous IFN-?, but not IFN-?, protected MCs against HRV infection.CONCLUSION AND CLINICAL RELEVANCE: MCs are permissive for the replication and release of HRV which is prevented by exogenous IFN-? treatment. Taken together these findings suggest a novel mechanism whereby MCs may contribute to HRV-induced asthma exacerbation
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