Effect of inhaled anesthetic to cultured cortical neurons
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ABSTRACT:
ORGANISM(S): Rattus norvegicus
PROVIDER: GSE2982 | GEO | 2005/07/23
SECONDARY ACCESSION(S): PRJNA91929
REPOSITORIES: GEO
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Project description:Inhaled anesthetics produce many effects and bind to a large number of brain proteins, but it is not yet clear if this is accompanied by widespread changes in gene expression of the biological targets. Such changes in expression might implicate functionally important targets from the large pool of binding targets. Isolated primary cortical neurons were exposed to anesthetics and DNA oligonucleotide microarrays were used to detect and quantify transcriptional changes in neuronal tissue. Experiment Overall Design: Primary cortical neurons were treated with 1MAC, 3MAC Halothane and 3MAC Isoflurane, together with no drug control. Pool no drug control was used as Cy3 channel in all chips. The above drug treated and individual control samples were used in Cy5 channel.
2008-05-07 | E-GEOD-2982 | biostudies-arrayexpress
Project description:Inhaled allergen challenge of subjects with allergic asthma allows the study of mechanisms involved in allergen-induced airway inflammation. The objective of this study was to identify changes in the plasma proteome associated with a late phase response (LPR) causing airway obstruction occurring 4-8 hours after the initial early response. Serial plasma samples from asthmatics undergoing inhaled allergen challenge were analyzed. Mass spectrometry data was analyzed using a linear regression to model the relationship between the degree of airway obstruction during the LPR and plasma proteome changes evoked by the inhaled allergen challenge. Inhaled allergen challenge induced changes in the plasma proteome including upregulation of the protease inhibitors alpha-1-antitrypsin, alpha-1-antichymotrypsin and plasma serine protease inhibitor. Out of 396 quantified proteins, 150 showed a statistically significant change 23 hours post allergen challenge. Further proteomic changes were associated with the LPR, including altered levels of coagulation factors such as an increased factor XII A and a decreased von Willebrand factor. Allergic reactions to inhaled allergens in asthmatic subjects was associated with changes in a large proportion of the measured plasma proteome, whereof protease inhibitors show the largest changes, likely to influence the inflammatory response. Of several other proteins altered in relation to the LPR, many are associated with coagulation.
2022-04-14 | PXD027091 | Pride
Project description:Inhaled corticosteroids (ICS) control airway inflammation in mild to moderate asthma by reducing inflammatory gene expression. However, incomplete understanding of the molecular mechanisms underpinning corticosteroid action hinders development of improved therapies for more severe disease. Microarray analysis was performed on RNA from biopsies taken from healthy individuals after receiving single dose of ICS to characterize corticosteroid-induced modulation of gene expression in the human airways. Healthy male, non-smoker, non-allergic volunteers (age 18-50 years) with normal lung function were recruited into a prospective, double-blind, placebo-controlled, randomized, two-period crossover study involving an initial screening visit, followed by two intervention visits. Participants were screened at visit 1 for fulfilment of the study eligibility criteria. At visit 2, volunteers were randomized to receive inhaled budesonide (1600 µg) or placebo, both via Turbuhaler. Two to three weeks later, at visit 3, participants received either budesonide or placebo, as appropriate to complete both study arms. Six hours after placebo or a budesonide inhalation, bronchial biopsies were obtained via bronchoscopy.
2016-06-11 | E-GEOD-83233 | biostudies-arrayexpress
Project description:Background: The first step in SARS-CoV-2 infection is binding of the virus to angiotensin converting enzyme 2 (ACE2) on the airway epithelium. Asthma affects over 300 million people world-wide, many of whom may encounter SARS-CoV-2. Epidemiologic data suggests that asthmatics who get infected may be at increased risk of more severe disease. Our objective was to assess whether maintenance inhaled corticosteroids (ICS), a major treatment for asthma, is associated with airway ACE2 expression in asthmatics. Methods: Large airway epithelium (LAE) of asthmatics treated with maintenance ICS (ICS+), asthmatics not treated with ICS (ICS-), and healthy controls (controls) was analyzed for expression of ACE2 and other coronavirus infection-related genes using microarrays. Results: AsResults: As a group, there was no difference in LAE ACE2 expression in all asthmatics vs controls. In contrast, subgroup analysis demonstrated that LAE ACE2 expression was higher in asthmatics ICS+ compared to ICS‾ and ACE2 expression was higher in male ICS+ compared to female ICS+ and ICS‾ of either sex. ACE2 expression did not correlate with serum IgE, absolute eosinophil level, or change in FEV1 in response to bronchodilators in either ICS- or ICS+. Conclusion: Airway ACE2 expression is increased in asthmatics on long-term treatment with ICS, an observation that should be taken into consideration when assessing the use of inhaled corticosteroids during the pandemic. a group, there was no difference in LAE ACE2 expression in all asthmatics vs controls. In contrast, subgroup analysis demonstrated that LAE ACE2 expression was higher in asthmatics ICS+ compared to ICS‾ and ACE2 expression was higher in male ICS+ compared to female ICS+ and ICS‾ of either sex. ACE2 expression did not correlate with serum IgE, absolute eosinophil level, or change in FEV1 in response to bronchodilators in either ICS- or ICS+. Conclusion: Airway ACE2 expression is increased in asthmatics on long-term treatment with ICS, an observation that should be taken into consideration when assessing the use of inhaled corticosteroids during the pandemic.
2021-07-15 | GSE179156 | GEO
Project description:The Differential Effects of Inhaled Symbicort and AdvaiR on Lung Microbiota (DISARM) study aimed to determine the effects of inhaled corticosteroids (ICS) on the lung microbiome. The full trial protocol is registered at clinicaltrials.gov (NCT02833480) and the study was approved by the Human Research Ethics Committee of the University of British Columbia and Providence Health Care (H14-02277). Participants were randomized to receive inhaled long-acting beta agonist (LABA) treatment with formoterol, or LABA/ICS combination treatment with formoterol/budesonide or salmeterol/fluticasone propionate, for 12 weeks. Bronchoscopy was performed before and after treatment, and bronchoalveolar lavage fluid and bronchial brushes (6th-8th generation) were collected. This dataset contains RNA-seq data from the bronchial brushes. RNA was extracted from cytological brush specimens stored in QIAzol RNA lysis buffer (QIAGEN, Stockach, Germany) using the RNeasy Plus kit (QIAGEN) according to the manufacturer’s instructions, and specimens were submitted for sequencing at the University of British Columbia Biomedical Research Centre. Sample quality control was performed using the Agilent 2100 Bioanalyzer (Agilent, Santa Clara, CA, USA). Qualifying samples were then prepared following the standard protocol for the NEBnext Ultra ii Stranded mRNA (New England Biolabs, Ipswich, MA, USA). Sequencing was performed on the Illumina NextSeq 500 (Illumina, San Diego, CA, USA) with paired end 42bp × 42bp reads. Samples were sequenced in batches of 24, with batches formed by random selection of samples.
2021-03-22 | GSE162120 | GEO
Project description:To identify key biological pathways that define susceptibility factors for pulmonary infection during obesity, diet-induced obese (DIO) and regular weight (RW) C57BL/6 mice were exposed to 0.5 µg/L inhaled lipopolysaccharide (LPS) for 1 hr/d for 4 days over a period of 2 weeks. Transcriptional responses were measured by global microarray analysis of lung tissue.
2012-09-15 | GSE38092 | GEO
Project description:Currently approved inhibitors of the PD-1/PD-L1 pathway represent a major advance for the treatment of lung cancers, yet they are ineffective in a majority of patients due to lack of pre-existing T cell reactivity. Here we show that a TLR9 agonist delivered by inhalation is able to prime T cell responses against poorly immunogenic lung tumors and to complement the effects of PD-1 blockade. Treatment with inhaled TLR9 agonist causes profound remodeling in tumor-bearing lungs, leading to formation of tertiary lymphoid structures adjacent to the tumors, CD8+ T cell infiltration into the tumors, dendritic cell expansion and antibody production. Inhaled TLR9 agonist treatment increased the pool of functional PD-1lowT-bethigh effector CD8+ T in tumor-bearing lungs. We show by transcriptional profiling, that the effector CD8+ T cells generated by inhaled TLR9 agonist treatment are licensed by PD-1 blockade to become highly functional CTL, leading to a durable rejection of both lung tumors and tumor lesions outside the lungs. CD4+ T cells activated in response to inhaled TLR9 play a critical role in this process by controlling the proliferation, preventing exhaustion, and guiding the differentiation of optimally functional CTL. This study characterizes a strategy to apply localized TLR9 stimulation to a tumor type not accessible for direct injection, a strategy that may expand the therapeutic potential of PD-1 blockade in non-small cell lung cancer. the scope of this experiment was to profile the gene expression of effector CD8 T cells from tumor bearing lungs treated by different drug regimen.
2018-05-04 | GSE113987 | GEO
Project description:Chronic LPS inhalation causes submucosal thickening and airway narrowing. To address the hypothesis that environmental airway disease is, in part, a fibroproliferative lung disease, we exposed C57BL/6 mice daily to LPS by inhalation for up to two months followed by one month of recovery. C57BL/6 mice exposed to daily inhaled LPS had significantly enhanced mRNA expression of TGF-beta1, TIMP-1, fibronectin-1, and pro-collagen types I, III, and IV and show prominent submucosal expression of the myofibroblast markers desmin and alpha-smooth muscle actin. To identify novel candidate genes that contribute to airway fibroproliferation, we performed microarray analysis on total lung RNA from mice exposed to LPS for one week. This analysis revealed a distinct subset of genes known to regulate ECM homeostasis. To further identify candidate genes specifically involved in generic fibroproliferation we interrogated this analysis with genes induced in C57BL/6 mouse lung by bleomycin. This analysis yielded a list of 212 genes in common. Prominent among which are genes know to be important in maintenance of bone homeostasis and which may play a central role in ECM homeostasis in the lung. These results suggest that there is a common subset of genes that regulate fibroproliferation in the lung independent of etiologic agent and site of injury. Keywords: mouse model of environmental airway disease; chronic LPS exposure
2008-03-01 | GSE8566 | GEO
Project description:Prohormone-derived neuropeptides act as cell-cell signaling molecules to mediate a wide variety of biological processes in the animal brain. Mass spectrometry-based peptidomic experiments are valuable approaches to gain insight into the dynamics of individual peptides under different physiological conditions or experimental treatments. However, the use of anesthetics during animal procedures may confound experimental peptide measurements, especially in the brain where anesthetics act. Here, we investigate the effect of the commonly used anesthetics isoflurane and sodium pentobarbital on the peptide profile in the rodent hypothalamus and cerebral cortex, as assessed by label-free quantitative peptidomics. Our results showed that neither anesthetic dramatically alters peptide levels, although extended isoflurane exposure did cause changes in a small number prohormone-derived peptides in the cerebral cortex. Overall, our results demonstrate that acute use of anesthetics can be used in peptidomic experiments of the hypothalamus and cerebral cortex without dramatic confounding of experimental results.
2023-10-25 | PXD043738 | Pride
Project description:Inhaled corticosteroids (ICS) control airway inflammation in mild to moderate asthma by reducing inflammatory gene expression. However, incomplete understanding of the molecular mechanisms underpinning corticosteroid action hinders development of improved therapies for more severe disease. Microarray analysis was performed on RNA from biopsies taken from healthy individuals after receiving single dose of ICS to characterize corticosteroid-induced modulation of gene expression in the human airways.
2016-06-11 | GSE83233 | GEO