Effect of Ozone on Airway Inflammation in Allergic Asthmatics Treated With Omalizumab
Status:
Terminated
Trial end date:
2007-07-01
Target enrollment:
Participant gender:
Summary
Ozone can cause acute airway inflammation in both asthmatics and normal volunteers. However,
in asthmatics ozone can cause episodes of worsening of asthma. We want to learn if chronic
allergic response, known as "IgE-induced airway inflammation" is what causes the increased
inflammation in response to ozone. To do this we will examine the response to ozone in a
group of asthmatics treated with omalizumab, a medicine available and approved for use in
people with asthma, or a placebo control. The placebo for this study is inert physiologic
saline ("salt water") which contains no omalizumab. Both the omalizumab and the placebo will
be administered as an injection under the skin. Omalizumab, also called Xolair, is a
humanized monoclonal antibody, which means that it originally was produced in mice, then
genetically engineered to look more like human than mouse antibody. Omalizumab inactivates
IgE, a protein our own immune systems make as part of allergic reactions. The purpose of this
study is to test the hypothesis that omalizumab, by blocking this aspect of allergic
reactions, will decrease the number of inflammatory cells in the airway after ozone
challenge. We also hypothesize that omalizumab will decrease the effects of ozone on changes
in lung function, mucociliary clearance (a measure of how quickly mucus clears form the
airway) and airway reactivity. Airway reactivity is a measure of how sensitive the airways
are to a medication used to diagnose asthma, called methacholine. We will examine these as
additional information we can learn during the course of the study. This is a blinded study,
meaning that neither you nor the researchers know if you get the active drug or placebo, but
that information can be obtained if needed. The placebo is an injection of inert
physiological saline ("salt water") which contains no omalizumab.
Phase:
N/A
Details
Lead Sponsor:
University of North Carolina, Chapel Hill
Collaborators:
Genentech, Inc. National Institutes of Health (NIH)