Autocrine activation of cultured macrophages by brain-derived neurotrophic factor

• Published in: Biochemical and biophysical research communications 2006-06, Vol.344 (3), p.941-947
• Main Authors: Asami, Toshio, Ito, Takuya, Fukumitsu, Hidefumi, Nomoto, Hiroshi, Furukawa, Yoshiko, Furukawa, Shoei
• Format: Article
• Language: English
• Subjects: Animals; Brain-derived neurotrophic factor (BDNF); Brain-Derived Neurotrophic Factor - administration & dosage; Brain-Derived Neurotrophic Factor - metabolism; Cells, Cultured; Culture; Dose-Response Relationship, Drug; Interleukin-1 - metabolism; Lipopolysaccharide (LPS); Macrophage Activation; Macrophages; Macrophages - drug effects; Macrophages - physiology; Mice; Neurotrophin 3 - administration & dosage; Neurotrophin-3 (NT-3); Phagocytic activity; Phagocytosis - drug effects; Phagocytosis - physiology; TrkB
• ISSN: 0006-291X; 1090-2104
• DOI: 10.1016/j.bbrc.2006.03.228

To elucidate a significance of the expression of brain-derived neurotrophic factor (BDNF) in the activated microglia/macrophages of the injured central nervous system, we examined BDNF actions on or BDNF synthesis by macrophages cultured from the mouse peritoneal cavity. They synthesized BDNF and neurotrophin-3 (NT-3) in addition to expressing high-affinity neurotrophin receptors, full-length TrkB (FL), truncated TrkB (TK −), and TrkC, thus suggesting an autocrine influence of BDNF and NT-3. BDNF, but not NT-3, enhanced phagocytic activity and stimulated synthesis/secretion of interleukin-1β in the same manner as lipopolysaccharide (LPS). Furthermore, there was a significant correlation of the phagocytic activity with the expression of BDNF or TrkB (FL). These results imply that the phagocytic activity of macrophages depends on BDNF synthesis and/or TrkB (FL) expression, suggesting that BDNF participates in the activation processes of macrophages by acting in an autocrine manner.