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Interferon‐γ Mediates Neuronal Killing of Intracellular Bacteria
Author(s) -
Jin Y.,
Lundkvist G.,
Dons L.,
Kristensson K.,
Rottenberg M. E.
Publication year - 2004
Publication title -
scandinavian journal of immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.934
H-Index - 88
eISSN - 1365-3083
pISSN - 0300-9475
DOI - 10.1111/j.0300-9475.2004.01500.x
Subject(s) - biology , intracellular , intracellular parasite , neuron , microbiology and biotechnology , interferon , listeria monocytogenes , nitric oxide synthase , hippocampal formation , interferon gamma , bacteria , nitric oxide , cytokine , immunology , neuroscience , endocrinology , genetics
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 by Listeria 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.

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