Published ahead of print on May 11, 2006, doi:10.1164/rccm.200501-082PP
Am. J. Respir. Crit. Care Med., Volume 174, Number 4, August 2006, 367-372
A more recent version of this article appeared on August 15, 2006
Submitted on January 19, 2005
Accepted on May 10, 2006
Asthma? Is it Due to an Abnormal Airway Smooth Muscle Cell?
Peter Borger1*, Michael Tamm1, Judith L Black2, and Michael Roth3
1 Pulmonary Cell Research, Department of Research and Pulmonology, Department of Internal Medicine, University Hospital Basel, Basel, Switzerland,
2 Department of Pharmacology, University of Sydney, Sydney, Australia,
3 Pulmonary Cell Research, Department of Research and Pulmonology, Department of Internal Medicine, University Hospital Basel, Basel, Switzerland; The Woolcock Institute of Medical Research, University of Sydney, Sydney, Australia
* To whom correspondence should be addressed. E-mail: pieter.borger{at}unibas.ch.
Asthma is an airway disease highly prevalent in westernized countries and of unknown aetiology. Often asthma is associated with atopy, but not all atopic individuals are asthmatics. Some asthma patients outgrow symptoms, whereas many others acquire asthma later in life. Still other patients suffer from asthma their entire life. How can we explain these different patterns? It may be asthma should be regarded as the clinical manifestation of a group of diseases with similar pathology due to a common factor. In this perspective we propose that an aberrant phenotype of airway smooth muscle (ASM) cells could be sufficient to explain the pathology of asthma. We will argue an abnormal ASM cell is a prerequisite to the development of asthma. Our postulate is that inadequate levels of C/EBP , a protein that is pivotal for the suppression of both inflammation and proliferation responses, confer on ASM cells an activated phenotype that is more susceptible to mitogenic and contractile stimuli.
Key words: asthma, airway smooth muscle cell abnormality, CCAAT/Enhancer Binding Proteins
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