Imaging of translocator protein upregulation is selective for pro‐inflammatory polarized astrocytes and microglia
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Abstract Translocator protein (TSPO) expression is increased in activated glia, and has been used as a marker of neuroinflammation in PET imaging. However, the extent to which TSPO upregulation reflects a pro‐ or anti‐inflammatory phenotype remains unclear. Our aim was to determine whether TSPO upregulation in astrocytes and microglia/macrophages is limited to a specific inflammatory phenotype. TSPO upregulation was assessed by flow cytometry in cultured astrocytes, microglia, and macrophages stimulated with lipopolysaccharide (LPS), tumor necrosis factor (TNF), or interleukin‐4 (Il‐4). Subsequently, mice were injected intracerebrally with either a TNF‐inducing adenovirus (AdTNF) or IL‐4. Glial expression of TSPO and pro‐/anti‐inflammatory markers was assessed by immunohistochemistry/fluorescence and flow cytometry. Finally, AdTNF or IL‐4 injected mice underwent PET imaging with injection of the TSPO radioligand 18F‐DPA‐713, followed by ex vivo autoradiography. TSPO expression was significantly increased in pro‐inflammatory microglia/macrophages and astrocytes both in vitro, and in vivo after AdTNF injection (p < .001 vs. control hemisphere), determined both histologically and by FACS. Both PET imaging and autoradiography revealed a significant (p < .001) increase in 18F‐DPA‐713 binding in the ipsilateral hemisphere of AdTNF‐injected mice. In contrast, no increase in either TSPO expression assessed histologically and by FACS, or ligand binding by PET/autoradiography was observed after IL‐4 injection. Taken together, these results suggest that TSPO imaging specifically reveals the pro‐inflammatory population of activated glial cells in the brain in response to inflammatory stimuli. Since the inflammatory phenotype of glial cells is critical to their role in neurological disease, these findings may enhance the utility and application of TSPO imaging.
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TSPO is expressed in almost all CNS cells, including astrocytes, neurons and endothelial cells.
“Although increased TSPO expression has historically been mostly associated with microglial activation, TSPO is now known to be expressed in almost all CNS cells including astrocytes, neurons and endothelial cells [21–27], all of which may also be involved in, or be affected by neuroinflammation [28].”
From Pharmacological modulation of TSPO in microglia/macrophages and neurons in a chronic neurodegenerative model of prion disease (2023) · cites this paper as [26]
The Introduction says that, in the CNS, TSPO expression is confined to glial and ependymal cells, contrary to the claim that it is expressed in almost all CNS cells, including neurons. The Discussion does report endothelial TSPO expression, and the paper documents astrocytic expression, but neither supports the claim about neurons or nearly all CNS cells. Page numbers were not supplied in our copy. (LLM, conf=0.86)
Checked by a reasoning model — may be wrong.
Experimental — accuracy not yet measuredTSPO is expressed in glial and endothelial cells.
“along with the established presence in the glial and endothelial cells [26, 45]”
From Pharmacological modulation of TSPO in microglia/macrophages and neurons in a chronic neurodegenerative model of prion disease (2023) · cites this paper as [26]
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“Given that more recent evidence confirms TSPO expression in neurons [44], along with the established presence in the glial and endothelial cells [26, 45], we were keen to examine the contribution of neurons, glia and endothelial cells to TSPO signal in ME7 mice.”
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- Authors
- Pannell, M., Economopoulos, V., Wilson, T. C., Kersemans, V., Isenegger, P. G., Larkin, J. R., Smart, S., Gilchrist, S., Gouverneur, V., & Sibson, N. R.
- Affiliations
- Cancer Research UK (GB)
- University of Oxford (GB)
- Corresponding author
- Sibson, Nicola R.
- ORCID
- Venue
- Glia
- Publisher
- Wiley
- Published
- 2019-09-03
- Volume
- 68
- Issue
- 2
- Pages
- 280-297
- ISSN
- 0894-1491 (ISSN-L)
- 1098-1136
- PMC
- PMC6916298
- OpenAlex
- W2972082263
- Cited by
- 109
- References
- 48
- Citations by year
- 2026: 5 · 2025: 3 · 2024: 16 · 2023: 14 · 2022: 16 · 2021: 33 · 2020: 19 · 2019: 3
- FWCI
- 7.81
- Type
- journal article
- Language
- en
- Open access
- hybrid
- doi.org
- Licence
- Locations
- Glia (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- Funders
- Biotechnology and Biological Sciences Research Council (BB/P026311/1)
- Cancer Research UK (C5255/A12678, C5255/A15935, C5255/A16466)
- Medical Research Council Canada (CRUK/MRC Oxford Institute for Radiation Oncology)
- Schweizerischer Nationalfonds zur Förderung der Wissenschaftlichen Forschung (P2BSP2_178609)
- Topics
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Pharmacological Receptor Mechanisms and Effects
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuroscience and Neuropharmacology Research
- Keywords
- translocator protein (TSPO), neuroinflammation, astrocytes, microglia, macrophages, glial activation, pro-inflammatory phenotype, TSPO PET imaging, TNF-α, IL-4, lipopolysaccharide, anti-inflammatory phenotype
- MeSH terms
- Animals, Astrocytes, Carrier Proteins, Disease Models, Animal, Inflammation, Lipopolysaccharides, Macrophages, Neuroglia, Microglia, Positron-Emission Tomography, Mice
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