AMΦs have an organ-specific function to maintain surfactant homeostasis that is critical to alveolar stability and lung function. AMΦs poses unique features such as aerobic respiration, high anti-oxidant capacity, and AMΦs alone among the all tissue MΦs are adapted to aerobic environment. Inflammation of the lungs causes respiratory failure and interferes with life sustaining. Therefore, treatment of foreign antigens with AMΦs should be done without inflammatory response as much as possible. AMΦs originate from fetal monocytes, are long-lived cells and their maintenance depend on self-renewing. GM-CSF is essential for the development of AMΦs but not other tissue MΦs. Characteristics of GM-CSF-induced human monocyte-derived MΦs (GM-MΦs) is the same as that of human AMΦs, indicating that the GM-MΦs become a model of human AMΦs. Expression of PPAR in nucleus of AMΦs depends on GM-CSF, and is essential for the development of AMΦs. Here, recent findings on the origin and the essential role of GM-CSF-PPAR axis in the development, surfactant homeostasis and anti-inflammatory activity of AMΦs are reviewed.

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When influenza viruses infect to airway, it is thought that hypothiocyanous acid (HOSCN), an oxidant with anti-influenza virus activity,is produced by the catalysis of peroxidases such as myeloperoxidase (MPO) andlactoperoxidase (LPO).However, the actions of HOSCN on host cells are poorly understood. In this study, we examined the effects of HOSCN on the expression of cytokines in airway epithelial cells. Human airway epithelial (NCI-H292) cells were exposed to HOSCN that generated in LPO/glucose oxidase/SCN- culture system. The gene expression of cytokines was determined by quantitative polymerase chain reaction and the concentration of cytokines also was measured by ELISA method. We found that HOSCN induced the expression of pro-inflammatory cytokines such as IL-6, IL-8, TNF-, IL-1and M-CSF, but it did not doGM-CSF. The results suggest that HOSCN may contribute to the production of pro-inflammatory cytokines during influenza viral infection. And also it may impact on the balance of M1/M2 development of macrophages, because M-CSF plays an important role for the differentiation of macrophagestoward M2 phenotype.

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