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Surfactant protein A (SP-A) and SP-A-derived peptide attenuate chemotaxis of mast cells induced by human β-defensin 3

Uehara, Yasuaki, Takahashi, Motoko, Murata, Masaki, Saito, Atsushi, Takamiya, Rina, Hasegawa, Yoshihiro, Kuronuma, Koji, Chiba, Hirofumi, Hashimoto, Jiro, Sawada, Norimasa, Takahashi, Hiroki, Kuroki, Yoshio, Ariki, Shigeru
Biochemical and biophysical research communications 2017 v.485 no.1 pp. 107-112
chemotaxis, ears, edema, eosinophils, humans, inflammation, mast cells, models, permeability, rats, surfactants
Human β-defensin 3 (hBD3) is known to be involved in mast cell activation. However, molecular mechanisms underlying the regulation of hBD3-induced mast cell activation have been poorly understood. We previously reported that SP-A and SP-A-derived peptide 01 (SAP01) regulate the function of hBD3. In this study, we focused on the effects of SP-A and SAP01 on the activation of mast cells induced by hBD3. SAP01 directly bound to hBD3. Mast cell-mediated vascular permeability and edema in hBD3 administered rat ears were decreased when injected with SP-A or SAP01. Compatible with the results in rat ear model, both SP-A and SAP01 inhibited hBD3-induced chemotaxis of mast cells in vitro. Direct interaction between SP-A or SAP01 and hBD3 seemed to be responsible for the inhibitory effects on chemotaxis. Furthermore, SAP01 attenuated hBD3-induced accumulation of mast cells and eosinophils in tracheas of the OVA-sensitized inflammatory model. SP-A might contribute to the regulation of inflammatory responses mediated by mast cells during infection.