For the first time, Assistant Professor Takumi Kawasaki and colleagues at the Graduate School of Bioscience, Nara Institute of Science and Technology have shown that controlling the differentiation and metabolism of alveolar macrophages plays an important role in controlling asthma.

 Macrophages are a type of white blood cell that prey on and digest dead cells and pathogens, and induce inflammation.It is present in each tissue such as lung, spleen, and liver, and it is known that each tissue has a different function.Alveolar macrophages localized in the lung play functions such as defense against infection in the lung, removal of allergens, and maintenance of lung tissue homeostasis.Alveolar macrophages are macrophages characteristic of the lung, but their differentiation and in vivo regulation were unclear.

 Inositol phospholipid is a kind of trace amount of phospholipid in the living body, and its metabolic enzyme is called inositol phospholipid metabolizing enzyme (PIKfyve).In this study, in order to clarify the role of inositol phospholipid-metabolizing enzyme in macrophages in vivo, mice in which the enzyme was specifically deficient in macrophages were prepared and analyzed.As a result, it was clarified that in the undifferentiated state of alveolar macrophages, excessive inflammation could not be suppressed and the asthma symptoms caused by the mite-derived component were exacerbated.

 Furthermore, it was found that inositol phospholipid metabolizing enzymes regulate the differentiation of alveolar macrophages.We were also able to show for the first time that inositol phospholipid metabolism in alveolar macrophages plays an important role in the control of chronic inflammation.

 This study elucidated a part of the differentiation control mechanism of alveolar macrophages.We also found that the regulation of inositol phospholipid metabolism may suppress chronic inflammation such as asthma.

Paper information: [The EMBO Journal] Deletion of PIKfyve alters alveolar macrophage populations and exacerbates allergic inflammation in mice

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