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Interleukin-10 protects against inflammation-mediated degeneration of dopaminergic neurons in substantia nigra.
Neurobiol Aging. 2007 Jun; 28(6):894-906.NA

Abstract

Inflammation has been increasingly recognized to play an important role in the pathogenesis of Parkinson's disease (PD). Using immunocytochemistry and electron microscopy, we found that intranigral injection of lipopolysaccharide (LPS) caused marked microglial activation and a dose-dependent selective loss of dopaminergic neurons, which was mediated by apoptosis as evidenced by prominent TUNEL labeling. RNase protection assays revealed that mRNA for Bax, Fas and the pro-inflammatory cytokines interleukin (IL)-1α, IL-1β, IL-6 and tumor necrosis factor (TNF)-α were significant increased ipsilaterally in LPS-injected side of SN, while expression of the anti-apoptotic gene Bcl-2 was decreased. Osmotic pump infusion of IL-10, a global inhibitor of cytokine synthesis, protected against LPS-induced cell death of dopaminergic neurons, with a corresponding decrease in the number of activated microglia, suggesting that the reduction in microglia-mediated release of inflammatory mediators may contribute to the anti-inflammatory effect of IL-10. Our results provide evidence that LPS induces apoptotic cell death in SNpc, which is likely through the expression of Fas, Bax, caspase-3, and the pro-inflammatory cytokines.

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Authors+Show Affiliations

Arimoto T
Department of Anatomy and Neurobiology, University of Kentucky, Medical Center, KY 40536, USA; Environmental Health Sciences Division, National Institute for Environmental Studies, Tsukuba, Ibaraki, Japan.
Choi DY
No affiliation info available
Lu X
No affiliation info available
Liu M
No affiliation info available
Nguyen XV
No affiliation info available
Zheng N
No affiliation info available
Stewart CA
No affiliation info available
Kim HC
No affiliation info available
Bing G
No affiliation info available

MeSH

AnimalsApoptosisCytokinesImmunohistochemistryInflammationInterleukin-10LipopolysaccharidesMaleMicrogliaMicroscopy, ElectronParkinson DiseaseRNA, MessengerRatsRats, Sprague-DawleyReceptors, DopamineSubstantia Nigra

Pub Type(s)

Journal Article
Research Support, N.I.H., Extramural
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

21887889

Citation

Arimoto, Toyoko, et al. "Interleukin-10 Protects Against Inflammation-mediated Degeneration of Dopaminergic Neurons in Substantia Nigra." Neurobiology of Aging, vol. 28, no. 6, 2007, pp. 894-906.
Arimoto T, Choi DY, Lu X, et al. Interleukin-10 protects against inflammation-mediated degeneration of dopaminergic neurons in substantia nigra. Neurobiol Aging. 2007;28(6):894-906.
Arimoto, T., Choi, D. Y., Lu, X., Liu, M., Nguyen, X. V., Zheng, N., Stewart, C. A., Kim, H. C., & Bing, G. (2007). Interleukin-10 protects against inflammation-mediated degeneration of dopaminergic neurons in substantia nigra. Neurobiology of Aging, 28(6), 894-906. https://doi.org/10.1016/j.neurobiolaging.2006.04.011
Arimoto T, et al. Interleukin-10 Protects Against Inflammation-mediated Degeneration of Dopaminergic Neurons in Substantia Nigra. Neurobiol Aging. 2007;28(6):894-906. PubMed PMID: 21887889.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Interleukin-10 protects against inflammation-mediated degeneration of dopaminergic neurons in substantia nigra. AU - Arimoto,Toyoko, AU - Choi,Dong-Young, AU - Lu,Xin, AU - Liu,Mei, AU - Nguyen,Xuan V, AU - Zheng,Naiying, AU - Stewart,Charles A, AU - Kim,Hyoung-Chun, AU - Bing,Guoying, PY - 2011/9/6/entrez PY - 2007/6/1/pubmed PY - 2011/9/9/medline SP - 894 EP - 906 JF - Neurobiology of aging JO - Neurobiol Aging VL - 28 IS - 6 N2 - Inflammation has been increasingly recognized to play an important role in the pathogenesis of Parkinson's disease (PD). Using immunocytochemistry and electron microscopy, we found that intranigral injection of lipopolysaccharide (LPS) caused marked microglial activation and a dose-dependent selective loss of dopaminergic neurons, which was mediated by apoptosis as evidenced by prominent TUNEL labeling. RNase protection assays revealed that mRNA for Bax, Fas and the pro-inflammatory cytokines interleukin (IL)-1α, IL-1β, IL-6 and tumor necrosis factor (TNF)-α were significant increased ipsilaterally in LPS-injected side of SN, while expression of the anti-apoptotic gene Bcl-2 was decreased. Osmotic pump infusion of IL-10, a global inhibitor of cytokine synthesis, protected against LPS-induced cell death of dopaminergic neurons, with a corresponding decrease in the number of activated microglia, suggesting that the reduction in microglia-mediated release of inflammatory mediators may contribute to the anti-inflammatory effect of IL-10. Our results provide evidence that LPS induces apoptotic cell death in SNpc, which is likely through the expression of Fas, Bax, caspase-3, and the pro-inflammatory cytokines. SN - 1558-1497 UR - https://www.unboundmedicine.com/medline/citation/21887889/Interleukin_10_protects_against_inflammation_mediated_degeneration_of_dopaminergic_neurons_in_substantia_nigra_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S0197-4580(06)00140-0 DB - PRIME DP - Unbound Medicine ER -