ED2-positive perivascular phagocytes produce interleukin-1β during delayed neuronal loss in the facial nucleus of the rat

D. N. Angelov*, M. Walther, M. Streppel, O. Guntinas-Lichius, A. M. Van Dam, E. Stennert, W. F. Neiss

*Corresponding author for this work

Research output: Contribution to journalArticleAcademicpeer-review

Abstract

Injection of Fluoro-Gold (FG) into the whisker pad of rats yields stable retrograde labeling of facial motoneurons. Subsequent removal of 10 mm from all facial nerve branches permanently deprives the FG-labeled motoneurons from their targets and the motoneurons gradually die. Neuronal debris is phagocytized by two types of neuronophages: parenchymal microglia (monoclonal antibody [MAb] OX42-positive, MAb ED2-negative) and perivascular phagocytes (OX42-negative, ED2-positive). Because both types of neuronophages express major histocompatibility complex (MHC) class II glycoproteins (MAb OX6- positive), they are considered to be the potential antigen-presenting cells of the brain. To check this hypothesis, we tested whether both types of neuronophages also synthetize the co-stimulatory cytokine interleukin-1β (IL-1β) immunocytochemically visualized by MAbs SILK-5/6. Employing combined fluorescent visualization of antigens (OX6, ED2, and SILK-5/6) in sections containing fluorescent (FG-prelabeled) neuronophages, we found that, during slowly occurring neuronal loss, the vast majority of IL-1β immunoreactive neuronophages were of perivascular (ED2-positive) origin. We concluded that, during delayed neuronal death 'behind' an intact blood-brain barrier, the perivascular phagocytes were more likely to function as antigen-presenting cells than the parenchymal microglia.

Original languageEnglish
Pages (from-to)820-827
Number of pages8
JournalJournal of Neuroscience Research
Volume54
Issue number6
DOIs
Publication statusPublished - 15 Dec 1998

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