Artificial lung as an alternative to mechanical ventilation in COPD exacerbation.

is the increased expression of membrane CD11b in fibrocytes. The integrin CD11b (also known as complement receptor type 3, macrophage antigen-1 and aMb2), which is primarily expressed on neutrophils, macrophages and monocytes, is critical for the normal function of these cells and plays an important role in the development of inflammatory responses. CD11b is expressed in a low-affinity, inactive conformation in circulating leukocytes, but is rapidly upregulated on the cell surface during stimulusdependent activation [10]. The factors triggering upregulation of CD11b in fibrocytes and its biological significance are not known. One hypothesis is that the increased expression of CD11b in fibrocytes reflects their activation in the course of the inflammatory response, as in patients with PAH. As a consequence of CD11b upregulation, fibrocytes might display an increased capability to adhere to endothelial cells, extravasate and subsequently transmigrate into the surrounding interstitial tissue. Fibrocytes therefore can be proposed to play a critical role in the initiation and maintenance of inflammation in PAH, even though they are not detected in the lung tissues. A central question that remains to be answered is whether fibrocytes differentiate into myofibroblasts, or whether they transiently stimulate differentiation and proliferation of other progenitor cells or resident mesenchymal cells within the lung.