Macrophage Polarization in Inflammatory Diseases

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

In order to counteract the excessive inflammatory response, macrophages undergo apoptosis or polarize to an M2 phenotype to protect the host from excessive injury and facilitate wound healing [24] . For example, microarray analysis and transcriptional profiling of peripheral blood cells showed that typical M1 genes and M1-related genes were replaced by M2 signature during treatment or convalescence in patients with typhoid fever [25] . LPS, large molecules in the outer membrane of gram-negative bacteria, play a critical pro-inflammatory role in acute infections. As the infection persists, host may present a LPS-tolerant state, and macrophages are polarized to M2 phenotype. A recent study has confirmed that the p50 subunit of NF-κB served as the key regulator of M2-driven LPS-tolerant state in this transformation [26] . As the excessive injury is reduced, however, M2 phenotype macrophages also induce an immunosuppressive state, resulting in a more susceptible situation to re-infection, thus relapse may occur or a carrier state may be found.