Borger Peter, Tamm Michael, Black Judith L, Roth Michael
Pulmonary Cell Research Department of Research University of Basel, Hebelstrasse 20, 4031 Basel, Switzerland.
Am J Respir Crit Care Med. 2006 Aug 15;174(4):367-72. doi: 10.1164/rccm.200501-082PP. Epub 2006 May 11.
Asthma is an airway disease highly prevalent in westernized countries and of unknown etiology. Often, asthma is associated with atopy, but not all atopic individuals have asthma. Some patients with asthma 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 that asthma should be regarded as the clinical manifestation of a group of diseases with similar pathology due to a common factor. In this Pulmonary 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/EBPalpha, 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.
哮喘是一种在西方国家高度流行且病因不明的气道疾病。通常，哮喘与特应性相关，但并非所有特应性个体都患有哮喘。一些哮喘患者症状会随年龄增长而消失，而许多其他人则在晚年患上哮喘。还有一些患者终生患有哮喘。我们如何解释这些不同的模式呢？可能是哮喘应被视为由一个共同因素导致的一组具有相似病理的疾病的临床表现。在本期《肺部视角》中，我们提出气道平滑肌（ASM）细胞的异常表型足以解释哮喘的病理。我们将论证异常的ASM细胞是哮喘发病的先决条件。我们的假设是，C/EBPα水平不足，这种对抑制炎症和增殖反应都至关重要的蛋白质，赋予了ASM细胞一种更易受促有丝分裂和收缩刺激影响的活化表型。
