Secondly, we cannot exclude the possibility that atherothrombotic material was selectively aspirated from the total of atherothrombotic material in situ. In our view, this cannot be the sole explanation for the observed histopathological features of the aspirated thrombus. Thirdly, additional immunostaining to optimize visualization of smooth muscle cells in specimen of lytic or organized thrombus was not performed. The major distinction in our paper, though, is fresh versus lytic or organized thrombus, which is not affected by this limitation. Finally, full information regarding anginal symptoms in the days or weeks before the acute myocardial infarction was not available. However, our previous thrombectomy study showed no clear relation between thrombus age and the presence or absence of Ceftizoxime preinfarction angina. The proximal airway epithelium is in contact with the environment and, as such, is at constant jeopardy from environmental injury. An efficient mechanism for airway repair is therefore essential to protect the host. Our current understanding of proximal airway repair is that a progenitor cell pool is located in the submucosal glands and submucosal gland ducts that are capable of self renewal and of differentiating in to the proximal airway subtypes e.g. mucus and ciliated cells. These progenitor cells express the immature cytokeratins CK5 and CK14 and move up the submucosal gland ducts to form the basal layer of the pseudostratified columnar epithelium of the proximal airway. From there the basal cells lose CK5/14 and gain more mature cytokeratins e.g. CK8/18 as they differentiate and move apically. We have shown the presence of circulating CK5 expressing cells that contributed to airway repair in a mouse model of ischemic injury and proximal airway repair. We used FACS analysis to show the presence of CK5 expressing cells in the bone marrow and circulation of mice. The identification of circulating epithelial cells that contribute to airway repair represents a controversial paradigm shift in the current concept of airway repair and regeneration after injury. The overall aims of this study were to determine whether CK5 mRNA expression could be quantified in the circulation of normal human subjects and to determine whether CK5 mRNA levels would be altered with severe airway disease,Chlorotetracycline such as in lung transplant patients with end stage lung disease. We also hypothesized that CK5 mRNA expression levels would increase as patients recovered post lung transplant and could function as a clinical biomarker of airway disease. Building on our previous studies on CK5 expressing circulating epithelial progenitor cells in the circulation, our present findings demonstrate the presence of CK5-positive cells in circulation in normal human subjects. Furthermore, they correlate the levels of CK5 in circulation with lung status post transplant. The significant reduction in CK5 expressing cells in the circulation of lung transplant patients argues that there may be a role for circulating epithelial progenitor cells in normal airway repair. This is further emphasized by the correlation that was found between an increase in circulating epithelial progenitor cells and an improvement in lung function after transplantation. Together, these results are consistent with the view that circulating epithelial progenitor cells may be critical for normal airway repair and that a lack of circulating epithelial progenitor cells may be associated with airway disease.