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Surfactant Protein A Leads to Monocytes Differentiation Through Activation of Cytoskeletal Signaling
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A4724 - Surfactant Protein A Leads to Monocytes Differentiation Through Activation of Cytoskeletal Signaling
Author Block: R. Takamiya, M. Murata, S. Ariki, A. Saito, N. Sawada, M. Takahashi, Y. Kuroki; Sapporo Medical University, Sapporo, Hokkaido, Japan.
Recent studies indicated that tissue-resident macrophages from embryonic progenitors can reside into adulthood and self-renewing by local proliferation. However, the mechanisms by which the local tissue environment regulates the function of alveolar macrophages is yet to be determined. On the other hand, pulmonary surfactant protein (SP)-A and SP-D are members of collectin family, and mediates the host-defense function during inflammation and infection through enhancing macrophage function. However, the relationship between SP and alveolar macrophage differentiation has not fully been understood. In this study, we hypothesised that SP may affect the function of monocytes. Human monocytic leukemia, THP-1 cells produced IL-8 in response to SP-A, but not to SP-D. In addition, SP-A induced cytoskeletal signaling, the phosphorylation of Rac1/cdc42 at serine-71 in THP-1 cells. Electron microscopy revealed that SP-A evoked the morphological changes with cytoplasmic protrusions. The cell migration assay indicated that SP-A increased the migratory potential of THP-1 cells. SP-A also increased the expression of transcription factor, PU.1 and junctional adhesion molecule (JAM)-A in THP-1 cells. Next, to determine whether SP-A affected the cell surface marker of macrophage. Flow cytometric analysis indicated that SP-A enhanced the expression of CD11b and F4/80, which surface marker of macrophage, on THP-1 cells. Next, we determined the phenotype of leukocyte in the lung of SP-A deficient (SP-A-/-) mice. Although a leukocyte common antigen, CD45 staining was not different in the lungs of SP-A+/+ and SP-A-/- mice, the expression of Siglec F and PU.1, which marker of alveolar macrophages, was reduced in the lung of SP-A-/- mice compared with SP-A+/+. These results suggest that SP-A may have a critical role in the differentiation of alveolar macrophages.
Author Block: R. Takamiya, M. Murata, S. Ariki, A. Saito, N. Sawada, M. Takahashi, Y. Kuroki; Sapporo Medical University, Sapporo, Hokkaido, Japan.
Recent studies indicated that tissue-resident macrophages from embryonic progenitors can reside into adulthood and self-renewing by local proliferation. However, the mechanisms by which the local tissue environment regulates the function of alveolar macrophages is yet to be determined. On the other hand, pulmonary surfactant protein (SP)-A and SP-D are members of collectin family, and mediates the host-defense function during inflammation and infection through enhancing macrophage function. However, the relationship between SP and alveolar macrophage differentiation has not fully been understood. In this study, we hypothesised that SP may affect the function of monocytes. Human monocytic leukemia, THP-1 cells produced IL-8 in response to SP-A, but not to SP-D. In addition, SP-A induced cytoskeletal signaling, the phosphorylation of Rac1/cdc42 at serine-71 in THP-1 cells. Electron microscopy revealed that SP-A evoked the morphological changes with cytoplasmic protrusions. The cell migration assay indicated that SP-A increased the migratory potential of THP-1 cells. SP-A also increased the expression of transcription factor, PU.1 and junctional adhesion molecule (JAM)-A in THP-1 cells. Next, to determine whether SP-A affected the cell surface marker of macrophage. Flow cytometric analysis indicated that SP-A enhanced the expression of CD11b and F4/80, which surface marker of macrophage, on THP-1 cells. Next, we determined the phenotype of leukocyte in the lung of SP-A deficient (SP-A-/-) mice. Although a leukocyte common antigen, CD45 staining was not different in the lungs of SP-A+/+ and SP-A-/- mice, the expression of Siglec F and PU.1, which marker of alveolar macrophages, was reduced in the lung of SP-A-/- mice compared with SP-A+/+. These results suggest that SP-A may have a critical role in the differentiation of alveolar macrophages.
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