Dysregulated Functions of Lung Macrophage Populations in COPD

Figure 2

Lung macrophage population functions in COPD. AMs exhibit alterations in their physiological responses in COPD; the secretion of proinflammatory cytokines and chemokines is dysregulated (1). The cells undergo oxidative stress and secrete ROS and nitrite species into the lung micro-environment (2), they store intracellularly large amounts of iron (2), and they overexpress and release proteases which cause alveolar tissue destruction (3). In contrast, processes, such as phagocytosis of microbes (4) and apoptotic neutrophils or epithelial cells (5), are downregulated in AMs from patients with COPD, an observation which could explain the frequent colonisation of the lungs with bacteria and viruses in exacerbations. In the meantime, monocytes are recruited from blood vessels following chemokine gradients and contribute to disease pathology via the secretion of proinflammatory mediators and proteases. It is also believed that monocytes differentiate into macrophages via an intermediate step of IMs which morphologically and functionally resemble monocytes.