Farm Animal Exposure, Respiratory Illnesses, and Nasal Cell Gene Expression
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ABSTRACT:
PROVIDER: PRJNA977716 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR24767700_1.fastq.gz | Fastqsanger.gz | |||
| SRR24767700_2.fastq.gz | Fastqsanger.gz | |||
| SRR24767701_1.fastq.gz | Fastqsanger.gz | |||
| SRR24767701_2.fastq.gz | Fastqsanger.gz | |||
| SRR24767702_1.fastq.gz | Fastqsanger.gz |
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Project description:Background: Farm exposures in early life reduce the risks for childhood allergic diseases and asthma. There is less information about how farm exposures relate to respiratory illnesses and mucosal immune development. Objective: We hypothesized that children raised in farm environments have a lower incidence of viral illnesses over the first two years of life than non-farm children. We also analyzed between farm exposures or respiratory illnesses were related to patterns of nasal cell gene expression. Methods: The Wisconsin Infant Study Cohort (WISC) birth cohort enrolled farm and non-farm pregnant women from central Wisconsin. Parents reported prenatal farm and other environmental exposures. Illness frequency and severity were assessed using illness diaries and periodic surveys. Nasopharyngeal cell gene expression at age two years was compared to farm exposure and respiratory illness history. Results: There was a higher rate of respiratory illnesses in the non-farm vs. farm group (rate ratio 0.82 [0.69,0.97], p=0.020), but no significant differences in wheezing illnesses. There was a stepwise reduction in rates of respiratory illnesses in children exposed at least weekly to 0, 1, or ≥2 animals (p=0.006). In analyzing nasal cell gene expression, farm exposures and preceding respiratory illnesses were positively related to gene signatures for mononuclear cells and innate and antimicrobial responses. Conclusions: Children exposed to farms and farm animals had lower rates of respiratory illnesses over the first two years of life. Both farm exposures and preceding respiratory illnesses were associated with increased innate immune responses, suggesting that these exposures stimulate mucosal immune responses to reduce subsequent illness frequency.
2024-01-29 | GSE233761 | GEO
Project description:Hydrogen sulfide (H2S) is a naturally occurring gas that is also associated with several industries. The potential for widespread human inhalation exposure to this toxic gas is recognized as a public health concern. The nasal epithelium is particularly susceptible to H2S-induced pathology. Injury to and regeneration of the nasal respiratory mucosa occurred in animals with ongoing H2S exposure suggesting that the regenerated respiratory epithelium undergoes an adaptive response and becomes resistant to further H2S induced toxicity. To better understand this adaptive response, twenty-four naive 10-week old male Sprague-Dawley rats were exposed to air or 200 ppm H2S in a nose-only exposure system for 3h/d for 1 or 5 consecutive days. Nasal respiratory epithelial cells at the site of injury and regeneration were laser capture microdissected and gene expression profiles were generated at time 3h, 6h, 24h, and 144h post initial exposure using the Affymetrix Rat Genome 430 2.0 microarray. Gene ontology enrichment analysis identified early gene changes in such functional categories as signal transduction, inflammatory/defense response, cell cycle, and response to oxidative stress. Later gene changes occurred in categories involved in cell cycle, DNA repair, transport, and micro-tubule-based movement. These data contribute to our understanding of the nasal epithelial cells? response to inhaled environmental toxicants. A better understanding of the H2S cytotoxicity mechanism will improve human risk assessment. Experiment Overall Design: Twenty-four naive 10-week old male Sprague-Dawley rats were exposed to air or 200 ppm H2S in a nose-only exposure system for 3h/d for 1 or 5 consecutive days. Nasal respiratory epithelial cells at the site of injury and regeneration were laser capture microdissected and gene expression profiles were generated at time 3h, 6h, 24h, and 144h post initial exposure using the Affymetrix Rat Genome 430 2.0 microarray.
2009-10-18 | E-GEOD-5349 | biostudies-arrayexpress
Project description:Exposure to cigarette smoke (CS) is etiologically linked to the development of fatal respiratory diseases, and there is a need to understand the mechanisms whereby CS causes damage. While animal models have provided valuable insights into smoking-related respiratory tract damage, modern toxicity testing calls for reliable in vitro models as alternatives for animal experimentation. Primary cells and immortalized cell lines can be used to gain some insight; however, the three-dimensional organotypic culture systems probably better mimic the morphological, physiological, and molecular attributes of the human respiratory tract. Even though the bronchus, bronchioles, and lung parenchyma are the primary sites of smoking-related respiratory disease manifestation, the nasal epithelium has been proposed as a surrogate tissue to study the effects of smoking on the respiratory tract. Here, we report on a repeated whole mainstream CS exposure of nasal and bronchial organotypic tissue cultures from which transcriptomic data were collected at several post-exposure time points. Despite the remarkably similar histology and cellular response to whole CS in both tissue types, as measured by cellular staining and cytokine secretion assessment, transcriptomic analyses combined with quantitative biological network modeling identified biological mechanisms that were unique to bronchial tissue at late post-exposure time points. Organotypic models therefore appear to be a promising alternative to animal experimentation, and provide species-relevant insights into the effects of CS exposure on the respiratory system.
2014-09-30 | E-MTAB-2250 | biostudies-arrayexpress
Project description:NSAID-exacerbated respiratory disease (N-ERD) represents a particularly severe endotype of chronic rhinosinusitis with nasal polyps (CRSwNP), which affects around 10-16% of CRSwNP patients. N-ERD is characterized by severe and refractory nasal polyposis, bronchial asthma and intolerance to non-steroidal anti-inflammatory drugs (NSAIDs), including aspirin. Today, the pathogenesis of N-ERD remains incompletely understood and curative treatments are lacking. Using a global transcriptomic approach, we identified local changes between the mucosa of N-ERD nasal polyps and healthy control inferior turbinates. Nasal brushing samples were collected from inferior turbinates of healthy controls and nasal polyps of N-ERD patients under anterior rhinoscopy and stored at -80°C in RNAprotect until RNA isolation and RNAseq.
2020-06-30 | E-MTAB-7962 | biostudies-arrayexpress
Project description:Background: In asthma, airway epithelium remodeling can already be detected during childhood, and epithelial cells are more susceptible to virus and oxidative stress. Their exact role in natural history and severity of children allergic respiratory disease remains however surprisingly unexplored. Aim: To analyze dysfunctions of epithelium in dust mite allergic respiratory disease (rhinitis ± asthma) in children. Methods: Expression profilings of nasal epithelial cells collected by brushing were performed on Affymetrix Hugene 1.0 ST arrays. All allergic patients were sensitized to dust mite. 19 patients had an isolated allergic rhinitis (AR). 14 patients had AR associated with asthma. Patients were compared to 12 controls, their severity and control being assessed according to NAEPP and ARIA criteria. Infections by respiratory viruses were excluded by real-time PCR measurements. Results: 61 probes were able to distinguish allergic rhinitis children from healthy controls. A majority of these probes was under the control of Th2 cytokines, as evidenced by parallel experiments performed on primary cultures of nasal epithelial cells. In uncontrolled asthmatic patients, we observed not only an enhanced expression of these Th2-responsive transcripts, but also a down-regulation of interferon-responsive genes. Conclusion: Our study identifies a Th2 driven epithelial phenotype common to all dust mite allergic children. Besides, it suggests that epithelium is involved in the severity of the disease. Expression profiles observed in uncontrolled asthmatic patients suggest that severity of asthma is linked at the same time to atopy and to impaired viral response. Nasal epithelium gene expression profiling of dust mite allergic children with isolated rhinitis, rhinitis associated with asthma and controls. 38 samples classified in 4 categories : 14 isolated rhinitis (R), 6 rhinitis with uncontrolled asthma (UA), 7 rhinitis with controlled asthma (CA) and 11 healthy subjects (C )
2012-01-05 | E-GEOD-19187 | biostudies-arrayexpress
Project description:The nasal epithelium is an important target site for chemically-induced toxicity and carcinogenicity. Human epidemiological investigations and experimental laboratory animal studies show that the nasal olfactory epithelium is selectively damaged by inhalation exposure to several chemicals, including vinyl acetate and hydrogen sulfide. The reason for the relative sensitivity of the nasal olfactory epithelium is not known. To better understand and predict the response of the nasal epithelium to inhaled xenobiotics, gene expression profiles from naÑve male and female Sprague-Dawley rats were constructed. Epithelial cells were manually collected from the nasal septum, naso- and maxillo-turbinates, and ethmoid turbinates of 9 male and 9 female rats. Gene expression analysis was performed using the Affymetrix Rat Genome 430 2.0 microarray. Gene ontology enrichment analysis identified several functional categories including xenobiotic metabolism, cell cycle, apoptosis, and ion channel/transport with significantly different expression between tissue types. Surprisingly, there were few gender differences in gene expression. This baseline data will contribute to our understanding of the normal physiology and selectivity of the nasal epithelial cellsâ response to inhaled environmental toxicants. Experiment Overall Design: To better understand and predict the response of the nasal epithelium to inhaled xenobiotics, gene expression profiles from naÑve male and female Sprague-Dawley rats were constructed. Epithelial cells were manually collected from the nasal septum, naso- and maxillo-turbinates, and ethmoid turbinates of 9 male and 9 female rats. Gene expression analysis was performed using the Affymetrix Rat Genome 430 2.0 microarray.
2008-06-13 | E-GEOD-5019 | biostudies-arrayexpress
Project description:Background: In asthma, airway epithelium remodeling can already be detected during childhood, and epithelial cells are more susceptible to virus and oxidative stress. Their exact role in natural history and severity of children allergic respiratory disease remains however surprisingly unexplored. Aim: To analyze dysfunctions of epithelium in dust mite allergic respiratory disease (rhinitis ± asthma) in children. Methods: Expression profilings of nasal epithelial cells collected by brushing were performed on Affymetrix Hugene 1.0 ST arrays. All allergic patients were sensitized to dust mite. 19 patients had an isolated allergic rhinitis (AR). 14 patients had AR associated with asthma. Patients were compared to 12 controls, their severity and control being assessed according to NAEPP and ARIA criteria. Infections by respiratory viruses were excluded by real-time PCR measurements. Results: 61 probes were able to distinguish allergic rhinitis children from healthy controls. A majority of these probes was under the control of Th2 cytokines, as evidenced by parallel experiments performed on primary cultures of nasal epithelial cells. In uncontrolled asthmatic patients, we observed not only an enhanced expression of these Th2-responsive transcripts, but also a down-regulation of interferon-responsive genes. Conclusion: Our study identifies a Th2 driven epithelial phenotype common to all dust mite allergic children. Besides, it suggests that epithelium is involved in the severity of the disease. Expression profiles observed in uncontrolled asthmatic patients suggest that severity of asthma is linked at the same time to atopy and to impaired viral response. Nasal epithelium gene expression profiling of dust mite allergic children with isolated rhinitis, rhinitis associated with asthma and controls.
2012-01-05 | GSE19187 | GEO
Project description:Assessment of host gene expression is an emerging tool for the diagnosis of human infections. We compared nasal and blood samples for evaluation of the host transcriptomic response in children with acute respiratory syncytial virus (RSV), symptomatic and asymptomatic picornavirus (PV) infection, and virus-negative asymptomatic controls (Ctrls). RNA was extracted from nasal and blood samples and analyzed by microarray. Despite generally lower quality of nasal RNA, the number of genes detected in each sample type was equivalent. Nasal gene expression signal derived mainly from epithelial cells but also included a leukocyte contribution that was higher in samples from symptomatic children. The number of genes with increased expression in virus-infected children was comparable in nasal and blood samples, while nasal samples also had large numbers of genes with decreased expression, including many genes associated with ciliary function and assembly. Compared to symptomatic children, those with asymptomatic PV had fewer genes with increased or decreased expression in both sample types. Genes with increased expression in comparisons of symptomatic children versus Ctrls included genes associated with components of innate immunity and apoptosis. Children with RSV but not PV also had increased expression of genes related to the cell cycle. Using nested leave-one-pair-out cross-validation and supervised principal components analysis, we defined sets of genes whose expression patterns accurately classified subjects, with high area-under-the-curve values in receiver operating characteristic analysis. Our results support use of nasal samples to augment pathogen-based tests to diagnose viral respiratory infection.
2019-01-01 | GSE117827 | GEO
Project description:Hydrogen sulfide (H2S) is a naturally occurring gas that is also associated with several industries. The potential for widespread human inhalation exposure to this toxic gas is recognized as a public health concern. The nasal epithelium is particularly susceptible to H2S-induced pathology. Injury to and regeneration of the nasal respiratory mucosa occurred in animals with ongoing H2S exposure suggesting that the regenerated respiratory epithelium undergoes an adaptive response and becomes resistant to further H2S induced toxicity. To better understand this adaptive response, twenty-four naive 10-week old male Sprague-Dawley rats were exposed to air or 200 ppm H2S in a nose-only exposure system for 3h/d for 1 or 5 consecutive days. Nasal respiratory epithelial cells at the site of injury and regeneration were laser capture microdissected and gene expression profiles were generated at time 3h, 6h, 24h, and 144h post initial exposure using the Affymetrix Rat Genome 430 2.0 microarray. Gene ontology enrichment analysis identified early gene changes in such functional categories as signal transduction, inflammatory/defense response, cell cycle, and response to oxidative stress. Later gene changes occurred in categories involved in cell cycle, DNA repair, transport, and micro-tubule-based movement. These data contribute to our understanding of the nasal epithelial cells? response to inhaled environmental toxicants. A better understanding of the H2S cytotoxicity mechanism will improve human risk assessment. Keywords: Time course
2008-07-01 | GSE5349 | GEO
Project description:Changes in the human nasal microbiome following exposure to pig farm environment: a prospective cohort study
| PRJEB24042 | ENA