epidermal-growth-factor has been researched along with Respiratory-Sounds* in 4 studies
1 trial(s) available for epidermal-growth-factor and Respiratory-Sounds
Article | Year |
---|---|
The effect of carvacrol on inflammatory mediators and respiratory symptoms in veterans exposed to sulfur mustard, a randomized, placebo-controlled trial.
The aim of this study was to evaluate the effect of carvacrol on serum level of inflammatory mediators and respiratory symptoms in the veterans exposed to sulfur mustard (SM).. Twenty-one patients who were exposed to SM more than two decades' ago were divided to placebo and carvacrol (1.2 mg/kg/day) treated groups. Serum levels of Tumor Necrosis Factor-α (TNF-α), Monocyte chemotactic protein-1 (MCP-1), Vascular endothelial growth factor (VEGF), Epidermal growth factor (EGF), forced expiratory volume-one second (FEV. FEV. Two months' treatment with carvacrol reduced inflammatory cytokine and chemokine while increased anti-inflammatory cytokines and improved respiratory symptom and FEV. This trial was registered under IRCT2014031617020N1 at http://www.irct.ir/. Topics: Chemokine CCL2; Chemokines; Cough; Cymenes; Cytokines; Epidermal Growth Factor; Forced Expiratory Volume; Humans; Inflammation Mediators; Inhalation Exposure; Middle Aged; Mustard Gas; Placebos; Respiratory Function Tests; Respiratory Sounds; Respiratory Tract Diseases; Terpenes; Tumor Necrosis Factor-alpha; Vascular Endothelial Growth Factor A; Veterans | 2019 |
3 other study(ies) available for epidermal-growth-factor and Respiratory-Sounds
Article | Year |
---|---|
Cluster analysis of nasal cytokines during rhinovirus infection identifies different immunophenotypes in both children and adults with allergic asthma.
Infection with rhinovirus (RV) is a major risk factor for disease exacerbations in patients with allergic asthma. This study analysed a broad set of cytokines in the noses of children and adults with asthma during RV infection in order to identify immunophenotypes that may link to virus-induced episodes.. Nasal wash specimens were analysed in children (n = 279 [healthy, n = 125; stable asthma, n = 64; wheeze, n = 90], ages 2-12) who presented to a hospital emergency department, and in adults (n = 44 [healthy, n = 13; asthma, n = 31], ages 18-38) who were experimentally infected with RV, including a subset who received anti-IgE. Cytokines were measured by multiplex bead assay and data analysed by univariate and multivariate methods to test relationships to viral load, allergic status, airway inflammation, and clinical outcomes.. Analysis of a core set of 7 cytokines (IL-6, CXCL8/IL-8, IL-15, EGF, G-CSF, CXCL10/IP-10 and CCL22/MDC) revealed higher levels in children with acute wheeze versus those with stable asthma or controls. Multivariate analysis identified two clusters that were enriched for acutely wheezing children; one displaying high viral load ("RV-high") with robust secretion of CXCL10, and the other displaying high IgE with elevated EGF, CXCL8 and both eosinophil- and neutrophil-derived mediators. Broader assessment of 39 cytokines confirmed that children with acute wheeze were not deficient in type 1 anti-viral responses. Analysis of 18 nasal cytokines in adults with asthma who received RV challenge identified two clusters; one that was "RV-high" and linked to robust induction of anti-viral cytokines and anti-IgE; and the other associated with more severe symptoms and a higher inflammatory state featuring eosinophil and neutrophil factors.. The results confirm the presence of different immunophenotypes linked to parameters of airway disease in both children and adults with asthma who are infected with RV. Such discrepancies may reflect the ability to regulate anti-viral responses. Topics: Adolescent; Adult; Asthma; Chemokine CXCL10; Child; Child, Preschool; Cluster Analysis; Cytokines; Enterovirus Infections; Epidermal Growth Factor; Granulocyte Colony-Stimulating Factor; Humans; Interleukin-15; Interleukin-6; Interleukin-8; Picornaviridae Infections; Respiratory Sounds; Rhinovirus; Young Adult | 2022 |
Increased epidermal growth factor in nasopharyngeal aspirates from infants with recurrent wheeze.
Airway remodeling is known to be a consequence of repeated injury and thought to be involved in early stage of asthma. We aimed to investigate the mediators associated with airway remodeling in recurrent early wheezers. Thirty-three infants, aged 2 years or less, admitted with exacerbation of wheezing were enrolled. All of them had experienced three or more episodes of wheezing before admission. They were categorized into two groups: those who had been hospitalized two or more times for severe wheezing (N = 19) and those who had only once or never been hospitalized (N = 14). Epidermal growth factor (EGF), vascular endothelial growth factor (VEGF), and transforming growth factor (TGF)-β1 levels in nasopharyngeal aspirates (NPA) collected on admission were measured. The difference between two patients groups divided based on their hospitalization history was assessed. We also examined these mediators in older asthmatic children (N = 15) admitted with exacerbation and their relationship with lung function parameters measured after stabilization. NPA EGF levels were significantly increased in recurrent early wheezers compared to controls. EGF, VEGF, and TGF-β1 levels were significantly higher in those with a previous history of multiple hospitalizations than in those without. In older asthmatic children, EGF levels were related with age and duration of asthma, but showed an inverse correlation with forced expiratory volume in 1 sec and forced expiratory flow between 25% and 75% of vital capacity. Our study shows that there might be significant damage during exacerbation in wheezy infants as levels of the mediators, EGF, VEGF, and TGF-β1 were higher in those who had been frequently hospitalized. It seems to suggest that those infants with severe recurrent wheezing might have chronic airway obstruction. Topics: Age Factors; Asthma; Case-Control Studies; Child, Preschool; Epidermal Growth Factor; Female; Forced Expiratory Flow Rates; Forced Expiratory Volume; Hospitalization; Humans; Infant; Male; Nasal Cavity; Pharynx; Recurrence; Respiratory Sounds; Transforming Growth Factor beta1; Vascular Endothelial Growth Factor A | 2015 |
Respiratory syncytial virus augments production of fibroblast growth factor basic in vitro: implications for a possible mechanism of prolonged wheezing after infection.
Respiratory syncytial virus (RSV) has been linked to the development of clinical asthma. Cellular mechanisms of this observation are not yet clearly elucidated. In chronic asthma, production of growth factors and remodeling are associated with prolonged wheezing. It was hypothesized that cells infected with RSV may produce excessive levels of fibroblast growth factor basic (FGFb), and epidermal growth factor (EGF). Airway epithelial cells were incubated with either: (i) virus, (ii) inactivated virus, or (iii) media only. The levels of FGFb and EGF were measured in the cellular supernatant fluid. The study demonstrated that by 24 h after RSV inoculation, or exposure to RSV-killed virus, cells are stimulated to produce significantly more FGFb, compared with non-infected/non-exposed control cells. FGFb is an important factor in remodeling and fibroblast activation in the airway. Using treatment with actinomycin D and cylcohexamide the effect of inhibiting translation or transcription in the infected cells, on FGFb production was demonstrated. There were no alterations in EGF production detectable. Based on the findings, the mechanism of FGFb secretion after RSV inoculation, appears to be regulated at the levels of both transcription and translation. The increased FGFb release potentially could contribute to fibroblast activation and remodeling in the airway, and thus provide another possible mechanism for prolonged wheezing after infection. Topics: Bronchi; Cell Survival; Dactinomycin; Epidermal Growth Factor; Epithelial Cells; Fibroblast Growth Factors; Humans; Protein Synthesis Inhibitors; Respiratory Sounds; Respiratory Syncytial Virus Infections; Respiratory Syncytial Viruses; Virus Inactivation; Virus Replication | 2003 |