Macrophage Polarization in Inflammatory Diseases

Liu, Yan-Cun; Zou, Xian-Biao; Chai, Yan-Fen; Yao, Yong-Ming

Asthma is a chronic inflammatory disease which is wide-spread in both developing and developed countries. Disorder in the regulation of phenotypes of pulmonary macrophages contributes to the pathogenesis of asthma [83] . It is widely accepted that M2 phenotype macrophages take a leading role in asthma, which they are beneficial for tissue repairing and restoration of homeostasis in the microenvironment of lung tissue. However, excessive M2 macrophages may increase cell recruitment and mucus secretion, and result in airway hyper-responsiveness. Moreira and colleagues transferred M2 phenotype macrophages into the lungs of fungus-induced asthmatic mice, then, both the inflammatory response and collagen deposition were enhanced, in turn accelerating the pathophysiological process of asthma [84] . With a boom in research of macrophage polarization, growing evidences support that M1 phenotype macrophages contribute to the development of asthma. In severe forms of asthma, especially in patients resistant to glucocorticoid therapy, macrophages are shown to become an M1 phenotype, which produces a great amount of pro-inflammatory mediators, including TNF-α, IL-1β, NO, exacerbates the lung injury and accelerate the airway remodeling [85] . For instance, NO produced by M1 phenotype leads to oxidative DNA damage and inflammation, enhances mucus production, and amplifies the lung injury in murine model of allergen-induced airway disease [86] . To sum up, regulation of the balance of macrophage polarization might provide a new way for the resolution of clinical asthma.