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Angiopoietin-like 4 Increases Pulmonary Vascular Leakiness and Lung Tissue Damage during Influenza Pneumonia

ABSTRACT: cANGPTL4 has been shown by our experiments to be associated to influenza-induced pneumonia pathogenesis. cANGPTL4 was produced in abundance during infection and inflammation and showed involvment in regulating blood vessel permeability. By using anti-cANGPTL4 monoclonal antibody, we want to see the overall effect of this antibody treatment, to evaluate the potential of anti-cANGPTL4 antibody as a possible treatment method for pneumonia, and also to gain more insight into the role of cANGPTL4 in infection and inflammation. We used microarrays to detail the global impact of anti-cANGPTL4 antibody treatment to see the possible mechanism pathways involved, as well as to identify the possible side effects caused by anti-cANGPTL4 antibody treatment to evaluate its potential as a treatment method.

ORGANISM(S): Mus musculus

PROVIDER: GSE58647 | GEO | 2015/06/20

SECONDARY ACCESSION(S): PRJNA253096

REPOSITORIES: GEO

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Angiopoietin-like 4 Increases Pulmonary Vascular Leakiness and Lung Tissue Damage during Influenza Pneumonia

Project description:cANGPTL4 has been shown by our experiments to be associated to influenza-induced pneumonia pathogenesis. cANGPTL4 was produced in abundance during infection and inflammation and showed involvment in regulating blood vessel permeability. By using anti-cANGPTL4 monoclonal antibody, we want to see the overall effect of this antibody treatment, to evaluate the potential of anti-cANGPTL4 antibody as a possible treatment method for pneumonia, and also to gain more insight into the role of cANGPTL4 in infection and inflammation. We used microarrays to detail the global impact of anti-cANGPTL4 antibody treatment to see the possible mechanism pathways involved, as well as to identify the possible side effects caused by anti-cANGPTL4 antibody treatment to evaluate its potential as a treatment method. Mouse lungs were harvested at different timepoints before and after antibody injection to see the changes caused by antibody injection as well as the overall trend during disease progression. To this end, we infected the mice and injected antibodies starting from day 13 post infection. We did the first harvest of lungs at day 12, before the antibody injection was started, to get a starting status to reflect the effect of antibody treatment. Samples harvested at day 14 post infection was analyzed to see the effect caused by antibody injection after 24 hours, and samples harvested at day 18 post infection was analyzed as the end point because our previous experiments showed significantly improved recovery at day 18 after antibody treatment.

2015-06-20 | E-GEOD-58647 | biostudies-arrayexpress

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Validation of the anti-Ro60 antibody (sc-100844, Sants Cruz Biotechnology, Inc) by coimmunoprecipitation from total HEK293 cell lysates

Project description:The mouse monoclonal anti-Ro60 antibody (sc-100844, Sants Cruz Biotechnology, Inc) has been validated by coimmunoprecipitation from total Flp-In T-REx 293 cell lysates. An anti-His antibody (SAB1305538, Sigma-Aldrich) was used as a negative control (see experimental details in Jeandard et al., "CoLoC-seq probes the global topology of organelle transcriptomes", manuscript in preparation). Ro60 was found to be the most strongly enriched protein (~23-fold enrichment). Low-level co-enrichment of other proteins (including mitochondria-localised ones) has also been observed. These data validate the specificity of the anti-Ro60 antibody.

2022-10-14 | PXD037383 | Pride

Mitochondrial dysfunction and immune response in pneumococcal pneumonia submitted to mechanical ventilation: impact of mesenchymal stem cells?

Project description:The goal of this study was to evaluate the impact of mechanical ventilation on immune and mitochondrial dysfunctions, in the setting of pneumococcal pneumonia in rabbits. Then, in a randomized trial, we assessed the effect of human umbilical cord-derived mesenchymal stem cells (MSCs), either alone, or in association with an atibiotic treatment (Ceftaroline) in the setting of pneumococcal pneumonia submitted to adverse mechanical ventilation. Pulmonary gene expression was analysed in an attempt to elucidate the effects of MSCs.

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RNASeq data from OMP-52M51 acute treated T-ALL PDX mice

Project description:We recently demonstrated that a human Notch1-specific neutralizing antibody (OMP-52M51) was very effective in T-ALL patient derived xenografts (PDX) bearing NOTCH1/FBW7 mutations. To evaluate the transcriptomic downstream effects of anti-NOTCH1 therapy, we perform RNA-Seq analysis in leukemia cells derived from PDTALL46 PDX mice after an acute treatment with control Ab or OMP-52M51.

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Single Cell Droplet-Based Efficacy and Transcriptomic Analysis of a Novel Anti-KLRG1 Antibody for Elimination of Autoreactive T Cells

Project description:Progress in developing improvements in the treatment of autoimmune disease has been gradual, due to challenges presented by the nature of these conditions. Namely, the need to suppress a patient’s immune response while maintaining the essential activity of the immune system in controlling disease. Targeted treatments to eliminate the autoreactive immune cells driving disease symptoms present a promising new option for major improvements in treatment efficacy and side effect management. Monoclonal antibody therapies can be applied to target autoreactive immune cells if the cells possess unique surface marker expression patterns. Killer cell lectin like receptor G1 (KLRG1) expression on autoreactive T cells presents an optimal target for this type of cell depleting antibody therapy. In this study, we apply a variety of in vitro screening methods to determine the efficacy of a novel anti-KLRG1 antibody at mediating specific natural killer (NK) cell mediated antibody-dependent cellular cytotoxicity (ADCC). The methods include single-cell droplet microfluidic techniques, allowing timelapse imaging and sorting based on cellular interactions. Included in this study is the development of a novel method of sorting cells using a droplet-sorting platform and a fluorescent calcium dye to separate cells based on CD16 recognition of cell-bound antibody. We applied this novel sorting method to visualize transcriptomic variation between NK cells that are or are not activated by binding the anti-KLRG1 antibody using RNA sequencing. The data in this study reveals a reliable and target-specific cytotoxicity of the cell depleting anti-KLRG1 antibody, and supports our droplet-sorting calcium assay as a novel method of sorting cells based on receptor activation.

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In vitro effect of the integrine LAMA4 on motility and cluster formation of human chondrocytes

Project description:Background: Cluster formation of hypertrophic chondrocytes is a sign of late stage osteoarthritis. In vitro chondrocytes have the ability to migrate on scaffolds. Important for motility issues in cartilage are integrines, part of the extracellular matrix, important for locomotory stimuli. The integrine Laminin4 is highly present in hypertrophic clusters of chondrocytes. We were interested if a blockade of LAMA4 is leading to less cluster formation. Methods: Human chondrocytes were cultured in a 2D matrixgel model and treated with different concentrations of a monoclonal anti-LAMA4-antibody.Migration habits were analysed using the cellobserver technique. An array analysis was performed before and after anti-LAMA4 treatment. The data set was screened for possible motility relevant genes. F-actin staining was performed to document cytoskeletal changes. Results: Anti-LAMA4 treatment reduced significantly the rate of cluster formation in human chondrocytes. Cells changed their surface promoting fewer extensions. Genes for motility and migration associated processes were differentially expressed by anti-LAMA4 treatment. Conclusion: LAMA4 blockade leads to less cluster formation in human chondrocytes in vitro. Anti-LAMA4 treatment suppresses filopodia expression, a possible explanation for less clustering. Interestingly anti-LAMA4 treatment seams to support a more milieu of earlier OA human chondrocytes were analysed untreated, IL-1 treated and 2A3 antibody treated

2015-12-22 | E-GEOD-68428 | biostudies-arrayexpress

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Project description:COVID-19, caused by SARS-CoV-2, is a virulent pneumonia, with >4,000,000 confirmed cases worldwide and >280,000 deaths as of May 13, 2020. It is critical to develop and evaluate vaccines and therapeutic interventions as rapidly as possible. Mice, the ideal animal for such studies, are resistant to SARS-CoV-2. Here, we overcome this difficulty by exogenous delivery of human ACE2 with a replication-deficient adenovirus (Ad5-hACE2). Ad5-hACE2-sensitized mice developed pneumonia characterized by weight loss, severe pulmonary pathology, and high-titer virus replication in lungs. Type I interferon, T cells and, most importantly, signal transducer and activator of transcription 1 (STAT1) are critical for virus clearance and diminished disease in these mice. Ad5-hACE2-transduced mice enabled rapid assessments of a vaccine candidate, of human convalescent plasma, and of two antiviral therapies (poly I:C and remdesivir). In summary, we describe a murine model of broad and immediate utility to investigate COVID-19 pathogenesis, and to evaluate new therapies and vaccines.

2020-06-11 | GSE150847 | GEO

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