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Histoblood Group Antigens as a Risk Factor of Asthma

This study has been completed.
National Heart, Lung, and Blood Institute (NHLBI)
Information provided by (Responsible Party):
University of California, San Francisco Identifier:
First received: September 16, 2005
Last updated: March 11, 2013
Last verified: March 2013
This study will evaluate the link between blood group antigens and asthma exacerbations.

Condition Intervention
Lung Diseases
Procedure: Screening

Study Type: Observational
Study Design: Observational Model: Case Control
Time Perspective: Prospective
Official Title: Histoblood Group Antigens, Viruses and Asthma

Further study details as provided by University of California, San Francisco:

Primary Outcome Measures:
  • Asthma exacerbations requiring prednisone [ Time Frame: Prior 2 years ]

Secondary Outcome Measures:
  • Lung fuction [ Time Frame: Current ]
    FEV1% predicted

Biospecimen Retention:   Samples With DNA
DNA, plasma, saliva, induced sputum.

Enrollment: 126
Study Start Date: July 2005
Primary Completion Date: August 2011 (Final data collection date for primary outcome measure)
Groups/Cohorts Assigned Interventions
Exacerbation resistant asthma
Control group
Procedure: Screening
Characterization tests including blood group typing, measures of lung function, measures of allergy, and collection of DNA.
Exacerbation prone asthma
Procedure: Screening
Characterization tests including blood group typing, measures of lung function, measures of allergy, and collection of DNA.

Detailed Description:


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.


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).


Ages Eligible for Study:   18 Years to 75 Years   (Adult, Senior)
Sexes Eligible for Study:   All
Accepts Healthy Volunteers:   No
Sampling Method:   Non-Probability Sample
Study Population
Asthmatics of two types: 1. Exacerbation resistant asthma (no requirement for prednisone for asthma since age 12). 2. Exacerbation prone asthma (requirement for prednisone for asthma in the past 2 years).

Inclusion Criteria:

  • Diagnosis of asthma, as confirmed by methacholine responsiveness less than 8 mg/mL
  • History of asthma exacerbation in the 2 years prior to study entry requiring treatment with oral corticosteroids

Exclusion Criteria:

  • Cigarette smoking in the 10 years prior to study entry or total pack per year history greater than 10
  • History of asthma exacerbations requiring treatment with oral corticosteroids since age 12 (control group)
  Contacts and Locations
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Please refer to this study by its identifier: NCT00201266

United States, California
University of California, San Francisco
San Francisco, California, United States, 94143
Sponsors and Collaborators
University of California, San Francisco
National Heart, Lung, and Blood Institute (NHLBI)
Study Chair: John V. Fahy University of California, San Francisco
  More Information

Publications automatically indexed to this study by Identifier (NCT Number):
Responsible Party: University of California, San Francisco Identifier: NCT00201266     History of Changes
Other Study ID Numbers: 283
R01HL080414 ( US NIH Grant/Contract Award Number )
Study First Received: September 16, 2005
Last Updated: March 11, 2013

Additional relevant MeSH terms:
Lung Diseases
Bronchial Diseases
Respiratory Tract Diseases
Lung Diseases, Obstructive
Respiratory Hypersensitivity
Hypersensitivity, Immediate
Immune System Diseases processed this record on May 23, 2017