Neurotrophin and Neurotrophin Receptor Expression in Alveolar Macrophages: An Immunocytochemical Study

• Published in: Growth factors (Chur, Switzerland) Switzerland), 2000, Vol.18 (3), p.193-202
• Main Authors: Ricci, Alberto, Greco, Stefania, Mariotta, Salvatore, Felici, Laura, Amenta, Francesco, Bronzetti, Elena
• Format: Article
• Language: English
• Subjects: Adult; Brain-Derived Neurotrophic Factor - metabolism; Female; human; Humans; immunocytochemistry; Immunohistochemistry; In Vitro Techniques; lung; Macrophages; Macrophages, Alveolar - immunology; Macrophages, Alveolar - metabolism; Male; Middle Aged; Nerve Growth Factor - metabolism; Nerve Growth Factors - metabolism; Neurotrophin 3 - metabolism; neurotrophins; Receptor, Nerve Growth Factor; Receptor, trkA - metabolism; Receptor, trkB - metabolism; Receptor, trkC - metabolism; receptors; Receptors, Nerve Growth Factor - metabolism
• ISSN: 0897-7194; 1029-2292
• DOI: 10.3109/08977190009003244

Abstract Alveolar macrophages play a crucial role in regulating lung immune responses and in maintaining the integrity of the respiratory tract. Neurotrophins (NTs), besides to their neurotrophic activities, exhibit physiological effects in the immune system. In this study, nerve growth factor (NGF), brain derived neurotrophic factor (BDNF), NT-3 and low- (p75) and high affinity (Trks) NT receptors were investigated by immunocytochemistry in cytospin centrifuged preparations of human alveolar macrophages. Approximately 2.5% alveolar macrophages were immunoreactive for NGF, whereas no macrophages displaying immunoreactivity for BDNF or NT-3 were observed. A 3.5% macrophages displayed immunoreactivity for TrkA-receptor protein, 10% for TrkB-receptor protein (full length isoform), and 2% for TrkC-receptor protein. No low-affinity p75 NT and TrkB[-] truncated isoform receptor immunoreactive macrophages were found. These findings support the hypothesis that NTs and the corresponding receptors may play a role in regulating immunological and functional activity of alveolar macrophages via paracrine/autocrine mechanisms.