Ignite Creation Date:
2024-05-05 @ 12:00 PM
Last Modification Date:
2024-10-26 @ 9:18 AM
Study NCT ID:
NCT00201266
Status:
COMPLETED
Last Update Posted:
2013-03-13
First Post:
2005-09-16
Brief Title:
Histoblood Group Antigens as a Risk Factor of Asthma
Sponsor:
University of California San Francisco
Organization:
University of California San Francisco
Study Overview
Official Title:
Histoblood Group Antigens Viruses and Asthma
Status:
COMPLETED
Status Verified Date:
2013-03
Last Known Status:
None
Delayed Posting:
No
If Stopped, Why?:
Not Stopped
Has Expanded Access:
False
If Expanded Access, NCT#:
N/A
Has Expanded Access, NCT# Status:
N/A
Acronym:
None
Brief Summary:
This study will evaluate the link between blood group antigens and asthma exacerbations
Detailed Description:
BACKGROUND
The purpose of this study is to explore the role of histoblood group antigens in virus-induced asthma exacerbations These antigens ABH and Lewis decorate O- and N-linked glycans on mucin and epithelial glycoproteins respectively Glycan synthesis involves glycosyltransferases including fucosyltransferases FUT encoded by FUT genes Glycan degradation involves glycosidases including fucosidase Secretor status is defined by FUT2 activity in epithelial cells which forms the H antigen and allows subsequent synthesis and secretion of A B and Lewis B antigens In preliminary studies it was found that 1 asthmatic patients with frequent exacerbations are more likely than non-exacerbated patients to be secretors 2 secretors report more frequently that a cold causes asthma and 3 sputum in stable asthma has abnormally high fucosidase activity These findings suggest that airway glycans are subjected to the following two competing homoeostatic influences 1 the diversity and activity of glycosyltransferases within cells that synthesize glycans and 2 the diversity and activity of glycosidases that turn over and remodel glycans in the airway lumen This study will test the hypothesis that secretor positive asthmatic patients are susceptible to virus-induced asthma exacerbation and that abnormal glycosidase activity in secretions modifies the glycan coat and promotes virus-induced exacerbation
DESIGN NARRATIVE
Secretor status will be studied in order to determine whether it is a risk factor for asthma exacerbations precipitated by viruses Preliminary studies suggest that secretor positive asthmatics are prone to asthma exacerbations and that asthmatic patients have abnormal glycosidase activity in their airway secretions This study will explore these findings further in the following two ways 1 a case-control study will compare secretor status and frequency of viral airway infection in 50 asthmatic patients hospitalized for management of acute severe asthma to 50 asthmatic subjects in the outpatient setting without a history of severe asthma exacerbation Sputum samples or tracheal aspirates from intubated patients will be collected from all patients In these samples DNA will be used as a microarray to detect viruses and 2 epithelial brushings and bronchial biopsies from a tissue bank will be used to establish the relationship between secretor status erythrocyte Lea and Leb phenotyping and airway epithelial cell activity of FUT genes real time RT-PCR and expression of Lea Leb A B and H antigens immunohistochemistry
The purpose of this study is to explore the role of histoblood group antigens in virus-induced asthma exacerbations These antigens ABH and Lewis decorate O- and N-linked glycans on mucin and epithelial glycoproteins respectively Glycan synthesis involves glycosyltransferases including fucosyltransferases FUT encoded by FUT genes Glycan degradation involves glycosidases including fucosidase Secretor status is defined by FUT2 activity in epithelial cells which forms the H antigen and allows subsequent synthesis and secretion of A B and Lewis B antigens In preliminary studies it was found that 1 asthmatic patients with frequent exacerbations are more likely than non-exacerbated patients to be secretors 2 secretors report more frequently that a cold causes asthma and 3 sputum in stable asthma has abnormally high fucosidase activity These findings suggest that airway glycans are subjected to the following two competing homoeostatic influences 1 the diversity and activity of glycosyltransferases within cells that synthesize glycans and 2 the diversity and activity of glycosidases that turn over and remodel glycans in the airway lumen This study will test the hypothesis that secretor positive asthmatic patients are susceptible to virus-induced asthma exacerbation and that abnormal glycosidase activity in secretions modifies the glycan coat and promotes virus-induced exacerbation
DESIGN NARRATIVE
Secretor status will be studied in order to determine whether it is a risk factor for asthma exacerbations precipitated by viruses Preliminary studies suggest that secretor positive asthmatics are prone to asthma exacerbations and that asthmatic patients have abnormal glycosidase activity in their airway secretions This study will explore these findings further in the following two ways 1 a case-control study will compare secretor status and frequency of viral airway infection in 50 asthmatic patients hospitalized for management of acute severe asthma to 50 asthmatic subjects in the outpatient setting without a history of severe asthma exacerbation Sputum samples or tracheal aspirates from intubated patients will be collected from all patients In these samples DNA will be used as a microarray to detect viruses and 2 epithelial brushings and bronchial biopsies from a tissue bank will be used to establish the relationship between secretor status erythrocyte Lea and Leb phenotyping and airway epithelial cell activity of FUT genes real time RT-PCR and expression of Lea Leb A B and H antigens immunohistochemistry
Study Oversight
Has Oversight DMC:
None
Is a FDA Regulated Drug?:
None
Is a FDA Regulated Device?:
None
Is an Unapproved Device?:
None
Is a PPSD?:
None
Is a US Export?:
None
Is an FDA AA801 Violation?:
None
Secondary IDs
| Secondary ID | Type | Domain | Link |
|---|---|---|---|
| R01HL080414 | NIH | None | httpsreporternihgovquickSearchR01HL080414 |