Abstract
ADA deficient mice as a model of eosinophilic pulmonary inflammation
Highlights
Adenosine deaminase (ADA) deficiency in humans causes a marked accumulation of adenosine and 2'-deoxyadenosine, which are associated with a variety of phenotypes including combined immunodeficiency, bony and renal abnormalities, hepatocellular damage, neurological disorders and pulmonary insufficiency
Adenosine has a well known role in asthma: elevated levels are found in the bronchoalveolar lavage fluids (BALF) from asthmatics; inhaled adenosine causes bronchoconstriction in asthmatics; airway inflammation is associated with altered expression of adenosine receptors; theophylline has a therapeutic role in asthma as an adenosine receptor antagonist
The authors conclude that this new animal model may help in better understanding human lung conditions in which eosinophils and macrophages are thought to play a pathogenic role, such as asthma, eosinophilic pneumonias, chronic obstructive pulmonary disease and emphysema
Summary
Adenosine deaminase (ADA) deficiency in humans causes a marked accumulation of adenosine and 2'-deoxyadenosine, which are associated with a variety of phenotypes including combined immunodeficiency, bony and renal abnormalities, hepatocellular damage, neurological disorders and pulmonary insufficiency. ADA deficient mice as a model of eosinophilic pulmonary inflammation Aff[1] S Maugeri Foundation, Veruno, (NO), Italy
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