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The lipopolysaccharide Parkinson’s disease animal model: mechanistic studies and drug discovery
Open accessAbstract
Research in the last two decades has unveiled an important role for neuroinflammation in the degeneration of the nigrostriatal dopaminergic (DA) pathway that constitutes the pathological basis of the prevailing movement disorder, Parkinson’s disease (PD). Neuroinflammation is characterized by the activation of brain glial cells, primarily microglia and astrocytes that release various soluble factors that include free radicals (reactive oxygen and nitrogen species), cytokines, and lipid metabolites. The majority of these glia‐derived factors are proinflammatory and neurotoxic and are particularly deleterious to oxidative damage‐vulnerable nigral DA neurons. As a proof of concept, various immunologic stimuli have been employed to directly induce glial activation to model DA neurodegeneration in PD. The bacterial endotoxin, lipopolysaccharide (LPS), has been the most extensively utilized glial activator for the induction of inflammatory DA neurodegeneration. In this review, we will summarize the various in vitro and in vivo LPS PD models. Furthermore, we will highlight the contribution of the LPS PD models to the mechanistic studies of PD pathogenesis and the search for neuroprotective agents for the treatment of PD.
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“Neuroinflammation is characterised by the activation of microglia and astrocytes [29].”
From Neuroprotective Effect of Ceftriaxone on MPTP‐Induced Parkinson’s Disease Mouse Model by Regulating Inflammation and Intestinal Microbiota (2021) · cites this paper as [29]
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“There is evidence suggesting that an uncontrolled sustained inflammation may lead to production of neurotoxic factors contributing to the pathogenesis of neurodegenerative diseases such as Alzheimer's disease and Parkinson's disease (Dutta et al., 2008; Glass et al., 2010; Qian etal., 2010).”
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“It is known that microglia may be activated by numerous factors, including LPS (Dutta, Zhang, and Liu 2008), methylmercury (MeHg) (Ni et al. 2012), manganese (Zhao et al. 2009), lead (Liu et al. 2012), and amyloid β (Doens and Fernandez 2014).”
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“Lipopolysaccharide (LPS), a bacterial endotoxin, can activate microglial inflammatory responses to induce degeneration of nigrostriatal dopamine neurons [6].”
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“Direct injection of LPS into the substantia nigra is used in experiments as a model of neurodegeneration in PD [3].”
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ResultSelf-citationWu, J., Yu, X., Xue, K., Wu, J., Wang, R., Xie, X., Li, K., Yang, Z., & Yue, J. (2020) · Oxidative Medicine and Cellular Longevity · doi:10.1155/2020/8735249 · Cited by 8
“The injection of lipopolysaccharide (LPS) into the SN region results in a progressive, specific, and irreversible loss of DA neurons and accumulation of α-synuclein [14].”
BackgroundAlpha-synuclein pathology enhances peripheral and CNS immune responses to bacterial endotoxins
Hartke, A.-S., Schreiber, C. S., Lau, K., Wiesweg, I., Waltl, I., Kalinke, U., Richter, F., & Käufer, C. (2024) · Neurobiology of Disease · doi:10.1016/j.nbd.2024.106773 · Cited by 8
“The LPS-induced murine inflammation model mimics these processes, including systemic and CNS inflammation and similar cytokine elevation profiles as detected in PD patients (Catorce and Gevorkian, 2016; Dutta et al., 2008).”
Mahnoor, M., Jahan, S., Elahi, L., Zakria, M., Rabia, R., Ikram, M. A., & Ullah, N. (2025) · Clinical and Experimental Pharmacology and Physiology · doi:10.1111/1440-1681.70043 · Cited by 7
Alterations of Gut Microbiota and Microbial Metabolites in Parkinson’s Disease: A Systematic Review
Davoody, S., Vakili, K. G., Jazi, K., Fathi, M., Heidari‐Foroozan, M., Mofidi, S. A., Taremi, M., Taherkhani, A., Azadnajafabad, S., Hojjatipour, F., et al. (2025) · Molecular Neurobiology · doi:10.1007/s12035-025-05598-7 · Cited by 7
“Studies have suggested that a decreased serum propionic acid level correlates with motor symptoms, cognitive ability, and a non-depression state [75, 76].”
Characterization of a SILAC method for proteomic analysis of primary rat microglia
Zhang, P., Culver‐Cochran, A. E., Stevens, S. M., & Liu, B. (2016) · PROTEOMICS · doi:10.1002/pmic.201500390 · Cited by 7
“2–5 ng/mL)-induced production of nitric oxide (NO), a reporter for the M1 microglial activation marker, inducible NO synthase (iNOS, [14]) (Fig.”
Self-citationβ-Funaltrexamine inhibits chemokine (CXCL10) expression in normal human astrocytes
Davis, R. L., Das, S., Buck, D. J., & Stevens, C. W. (2013) · Neurochemistry International · doi:10.1016/j.neuint.2013.01.013 · Cited by 7
“Others have reported that naloxone has anti-inflammatory and neuroprotective actions that are unrelated to MOR antagonism (Dutta et al., 2008; Liu et al., 2000; Liu et al., 2002; Zhang et al., 2010).”
BackgroundParkinson’s Disease and Parkin: Insights from Park2 Knockout Mice
Stephenson, S. E. M., Juliet, M., & Paul, J. (2012) · InTech eBooks · doi:10.5772/18148 · Cited by 6
“LPS is a bacterial endotoxin that is used as a glial activator for the induction of inflammatory dopaminergic neurodegeneration (Dutta et al., 2008).”
BackgroundMicroparticles Mediate Lipopolysaccharide-induced Inflammation and Chronic Pain in Mouse Model
Singh, A., Khushi, K., Tiwari, V., & Kumar, A. (2024) · NeuroMolecular Medicine · doi:10.1007/s12017-024-08809-x · Cited by 6
“Experimental studies have shown that bacterial lipopolysaccharide (LPS) can induce or accelerate neurodegeneration in mouse and rat models (Dutta et al., 2008).”
He, Y., & Lee, S. M. (2022) · Journal of Visualized Experiments · doi:10.3791/64313 · Cited by 5
Hobin, K., Costas‐Rodríguez, M., Wonterghem, E. V., Vandenbroucke, R. E., & Vanhaecke, F. (2022) · Frontiers in Chemistry · doi:10.3389/fchem.2022.896279 · Cited by 5
Llavero, F., Montoro, M. L., Sastre, A. A., Lacerda, H. M., & Zugaza, J. L. (2021) · International Journal of Molecular Sciences · doi:10.3390/ijms222312936 · Cited by 5
Katsipis, G., Lavrentiadou, S. N., Geromichalos, G. D., Tsantarliotou, M. P., Halevas, E. G., Litsardakis, G., & Pantazaki, Α. A. (2024) · International Journal of Molecular Sciences · doi:10.3390/ijms26010282 · Cited by 4
“Indeed, LPS induce neuropathological alterations in laboratory animals that mimic those observed in patients with AD or other neurodegenerative conditions [50,51].”
Mani, S., Bouchnak, H., Pradeloux, S., Kraı̈em, J., Soulet, D., & Messaoudi, I. (2023) · Clinical and Experimental Pharmacology and Physiology · doi:10.1111/1440-1681.13799 · Cited by 4
“The possible neuroprotective and neurorescue effects of the synthesized compound were tested: (i) in N27 dopaminergic and BV-2 microglial cell lines treated with 6-hydroxydopamine (6-OHDA) and (ii) in the 6-OHDA rat model of PD. PHAH administration reduced proinflammatory markers, including nitric oxide synthase and i…”
BackgroundInfluentialLong, J., Li, X., Yao, C., Liu, X., Li, N., Zhou, Y., Li, D., Su, S.-Q., Wang, L., Liu, H., et al. (2024) · Neuroscience Letters · doi:10.1016/j.neulet.2024.137800 · Cited by 4
Wang, T.-A., Li, S.-Y., Fann, L.-Y., Li, I., Liu, T., Hung, H.-Y., Chang, C.-W., Cheng, C., Huang, Y.-C., Yu, P.-Y., et al. (2025) · Journal of Central Nervous System Disease · doi:10.1177/11795735241312661 · Cited by 4
ESE-1 mediates lipopolysaccharide-induced BV2 cell inflammation via upregulation of HMGB1 expression
Lu, Y., Ding, J., Huang, J., & Zhao, Y. (2023) · Journal of Biosciences · doi:10.1007/s12038-023-00373-z · Cited by 3
“2007; Dutta et al .”
The role of CRMP4 in LPS-induced neuroinflammation
Asahina, R., Takahashi, M., Takano, H., Yao, R., Abe, M., Goshima, Y., & Ohshima, T. (2024) · Brain Research · doi:10.1016/j.brainres.2024.149094 · Cited by 3
Zhao, Y., Yang, X., Meng, F., & Li, W. (2020) · Canadian Journal of Physiology and Pharmacology · doi:10.1139/cjpp-2019-0699 · Cited by 3
Contribution of neuroinflammation, resolution, and neuroprotection in neuropsychiatric diseases
Farooqui, A. A. (2021) · Elsevier eBooks · doi:10.1016/b978-0-323-88460-0.00002-3 · Cited by 2
Liu, T., Liu, C., Li, I., Chu, Y.-C., Hung, H.-Y., Chiu, C.-H., Chou, T.-K., Li, S.-Y., Wang, T.-A., & Shih, J. (2025) · Behavioral and Brain Functions · doi:10.1186/s12993-025-00289-8 · Cited by 3
“…a bacterial endotoxin recognized by Toll-like receptor 4 (TLR4), robustly activates microglia and astrocytes, resulting in the release of pro-inflammatory cytokines (e.g., TNF-α, IL-1β), inducible nitric oxide synthase (iNOS), cyclooxygenase-2 (COX-2), and reactive oxygen/nitrogen species [13, 14].”
Immunity in Parkinson's disease – The role of innate responses
Iyengar, A. S., Dunkley, P. R., & Dickson, P. W. (2025) · Journal of Neuroimmunology · doi:10.1016/j.jneuroim.2025.578716 · Cited by 4
Contribution of neuroinflammation, resolution, and neuroprotection in neurodegenerative diseases
Farooqui, A. A. (2021) · Elsevier eBooks · doi:10.1016/b978-0-323-88460-0.00010-2 · Cited by 2
Development of a method for the isolation and culture of astrocytes from the canine cerebral cortex
Xue, Y.-J., Cui, S.-S., Guo, D., Liu, J., Yang, M., Kang, H., Jiang, Q., & Qu, L. (2022) · Journal of Neuroscience Methods · doi:10.1016/j.jneumeth.2022.109476 · Cited by 2
A Primary Neural Cell Culture Model for NeuroinflammationPreprint
Goshi, N., Morgan, R. K., Lein, P. J., & Şeker, E. (2020) · bioRxiv (Cold Spring Harbor Laboratory) · doi:10.1101/2020.01.23.914226 · Cited by 2
“, 2015), Parkinson’s disease (PD) (Dutta et al., 2008) and even mood disorders such as clinical depression (Henry et al.”
BackgroundKazanova, A., Sung, J., Oliveira, N., Gavino, C., Recinto, S. J., Bessaiah, H., Pei, J., Burns, L., Miller, W., Brouillard-Galipeau, M., et al. (2024) · bioRxiv (Cold Spring Harbor Laboratory) · doi:10.1101/2024.02.25.580545 · Cited by 2
“H. pylori can mediate chronic inflammation in certain individuals, and inflammation is increasingly implicated in PD (Dutta et al., 2008; Wei et al., 2024).”
BackgroundAfaar, F., Youssef, P., Galper, J., Chua, M., Halliday, G. M., Lewis, S. J. G., & Dzamko, N. L. (2025) · Movement Disorders · doi:10.1002/mds.30233 · Cited by 1
“17-19 Systemic activation of the innate immune system with lipopolysaccharide is commonly used to induce neurodegeneration in rodent models, 20,21 and higher levels of peripheral in fl ammatory cytokines may exacerbate the progression of PD. 22,23 In fl ammatory bowel disease (IBD) can increase the…”
Sandrine, M. N. Y., Owona, P. E., Ella, F. A., Bilanda, D. C., Julie, A. O. J., Cynthia, B. Y. P., Michel, B. G., Dzeufiet, P. D. D., Binsaleh, A. Y., Alwethaynani, M. S., et al. (2025) · Journal of Computational Biophysics and Chemistry · doi:10.1142/s2737416525501248 · Cited by 1
Copper regulates the expression of immune genes in microglial cells in vitro
Craciun, L., Muroy, S. E., & Saijo, K. (2025) · Immunobiology · doi:10.1016/j.imbio.2025.153145 · Cited by 3
“One compelling in vivo model involves stereotaxic injection of LPS into the substantia nigra—a procedure used by our group and others (Dutta et al., 2008; Saijo et al., 2009) to mimic neuroinflammation and Parkinson’s disease (PD) pathology.”
The role of microglia–lymphocyte interaction in PD neuropathology
Carta, A. R. (2012) · Basal Ganglia · doi:10.1016/j.baga.2012.07.003 · Cited by 1
MODELING OF PARKINSONISM SYNDROME IN RATS BY THE ADMINISTRATION OF LIPOPOLYSACCHARIDE
Boika, A. V., Гладкова, Ж. А., Kuznetsova, T. Y., & Ponomarev, V. V. (2018) · Journal of the Grodno State Medical University · doi:10.25298/2221-8785-2018-16-6-690-696 · Cited by 1
Metadata
- Authors
- Dutta, G., Zhang, P., & Liu, B.
- Affiliations
- University of Florida (US)
- Corresponding author
- Liu, Bin
- ORCID
- Liu, Bin
- Venue
- Fundamental & Clinical Pharmacology
- Publisher
- Wiley
- Published
- 2008-09-21
- Volume
- 22
- Issue
- 5
- Pages
- 453-464
- ISSN
- 0767-3981 (ISSN-L)
- 1472-8206
- PMC
- PMC2632601
- OpenAlex
- W2057913943
- Cited by
- 235
- References
- 106
- Citations by year
- 2026: 2 · 2025: 11 · 2024: 14 · 2023: 10 · 2022: 15 · 2021: 19 · 2020: 15 · 2019: 10 · 2018: 13 · 2017: 14 · 2016: 14 · 2015: 13 · 2014: 14 · 2013: 16 · 2012: 22
- FWCI
- 1.63
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Fundamental and Clinical Pharmacology (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Institute of Environmental Health Sciences (ES013265, R01ES013265)
- Topics
- Health Sciences › Medicine › Clinical Neurology › Parkinson's Disease Mechanisms and Treatments
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Nuclear Receptors and Signaling
- Keywords
- Parkinson's disease, lipopolysaccharide, neuroinflammation, nigrostriatal pathway, dopaminergic neuron loss, microglial activation, astrocytes, glial activation, neuroprotection, drug discovery, oxidative stress, cytokines, Parkinson's disease model
- MeSH terms
- Animals, Antiparkinson Agents, Disease Models, Animal, Humans, Lipopolysaccharides, Parkinson Disease, Drug Discovery
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