Macrophage Polarization in Inflammatory Diseases

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

Bacteria When tissues are challenged by pathogens, inflammatory monocytes in circulation are recruited and differentiated into macrophages, which keep a homeostatic status with the resident macrophages in the affected tissues. Generally, macrophages are deliberated to be polarized toward an M1 phenotype in the early stage of bacterial infection. When the pathogen associated molecular patterns (PAMPs) presented in bacteria are recognized by pathogen recognition receptors (such as Toll-like receptors, TLRs), macrophages are activated and produce a large amount of pro-inflammatory mediators including TNF-α, IL-1, and nitric oxide (NO), which kill the invading organisms and activate the adaptive immunity [11] . This mechanism has been considered to be involved in infection with Salmonella typhi, Salmonella typhimurium, Listeria monocytogenes [21] , and the early phases of infection with Mycobacterium tuberculosis, Mycobacterium ulcerans, and Mycobacterium avium [22] . If macrophage-mediated inflammatory response cannot be quickly controlled, a cytokine storm is formed, thereby contributing to the pathogenesis of severe sepsis [23] .