| Autor: |
Jin, Y., Lundkvist, G., Dons, L., Kristensson, K., Rottenberg, M. E. |
| Předmět: |
|
| Zdroj: |
Scandinavian Journal of Immunology; Nov2004, Vol. 60 Issue 5, p437-448, 12p |
| Abstrakt: |
Neurons can be targets for microbes, which could kill the neurons. Just in reverse, we, in this study, report that bacteria can be killed when entering a neuron. Primary cultures of foetal mouse hippocampal neurons and a neuronal cell line derived from mouse hypothalamus were infected byListeria monocytogenes. Treatment with interferon-γ (IFN-γ) did not affect bacterial uptake, but resulted in increased killing of intracellular bacteria, whereas the neuronal cell remained intact. The IFN-γ-mediated bacterial killing was mapped to the neuronal cytosol, before listerial actin tail formation. Treatment with IFN-γ induced phosphorylation of the transcription factor STAT-1 in neurons and IFN-γ-mediated listerial killing was not observed in STAT-1–/– neurons or neurons treated with IFN regulatory factor-1 antisense oligonucleotides. IFN-γ-treated neuronal cells showed increased levels of inducible nitric oxide synthase (iNOS) mRNA, and antisense iNOS oligonucleotides hampered the bacterial killing by neurons upon IFN-γ treatment. This novel neuronal function– i.e., that of a microbe killer– could play a crucial role in the control of infections in the immuno-privileged nervous system. [ABSTRACT FROM AUTHOR] |
| Databáze: |
Complementary Index |
| Externí odkaz: |
|
