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Lesion-associated microglia and macrophages mediate corralling and react with massive phagocytosis for debris clearance and wound healing after LPS-induced dopaminergic depletion.
Heman-Bozadas, P; Romero, C; Martínez-Remedios, P; Freitag, I; Frías, A; Saavedra-López, E; Casanova, P V; Roig-Martínez, M; Cribaro, G P; Rovirosa-Hernández, M J; Hernandez-Baltazar, D; Barcia, C.
Affiliation
  • Heman-Bozadas P; Institut de Neurociències & Department of Biochemistry and Molecular Biology, School of Medicine & School of Biosciences, Universitat Autònoma de Barcelona, Barcelona, Spain; Instituto de Neuroetología, Universidad Veracruzana, Xalapa, Veracruz, Mexico.
  • Romero C; Institut de Neurociències & Department of Biochemistry and Molecular Biology, School of Medicine & School of Biosciences, Universitat Autònoma de Barcelona, Barcelona, Spain.
  • Martínez-Remedios P; Institut de Neurociències & Department of Biochemistry and Molecular Biology, School of Medicine & School of Biosciences, Universitat Autònoma de Barcelona, Barcelona, Spain.
  • Freitag I; Institut de Neurociències & Department of Biochemistry and Molecular Biology, School of Medicine & School of Biosciences, Universitat Autònoma de Barcelona, Barcelona, Spain.
  • Frías A; Institut de Neurociències & Department of Biochemistry and Molecular Biology, School of Medicine & School of Biosciences, Universitat Autònoma de Barcelona, Barcelona, Spain.
  • Saavedra-López E; Institut de Neurociències & Department of Biochemistry and Molecular Biology, School of Medicine & School of Biosciences, Universitat Autònoma de Barcelona, Barcelona, Spain.
  • Casanova PV; Institut de Neurociències & Department of Biochemistry and Molecular Biology, School of Medicine & School of Biosciences, Universitat Autònoma de Barcelona, Barcelona, Spain.
  • Roig-Martínez M; Institut de Neurociències & Department of Biochemistry and Molecular Biology, School of Medicine & School of Biosciences, Universitat Autònoma de Barcelona, Barcelona, Spain.
  • Cribaro GP; Institut de Neurociències & Department of Biochemistry and Molecular Biology, School of Medicine & School of Biosciences, Universitat Autònoma de Barcelona, Barcelona, Spain.
  • Rovirosa-Hernández MJ; Instituto de Neuroetología, Universidad Veracruzana, Xalapa, Veracruz, Mexico.
  • Hernandez-Baltazar D; Instituto de Neuroetología, Universidad Veracruzana, Xalapa, Veracruz, Mexico; Cátedras CONACyT, Dirección Adjunta de Desarrollo Tecnológico e Innovación, Consejo Nacional de Ciencia y Tecnología. CDMX, Mexico.
  • Barcia C; Institut de Neurociències & Department of Biochemistry and Molecular Biology, School of Medicine & School of Biosciences, Universitat Autònoma de Barcelona, Barcelona, Spain. Electronic address: carlos.barcia@uab.es.
J Neuroimmunol ; 367: 577874, 2022 06 15.
Article in En | MEDLINE | ID: mdl-35490443
Neuroinflammation contributes to neuronal degeneration in Parkinson's disease (PD). However, how brain inflammatory factors mediate the progression of neurodegeneration is still poorly understood. Experimental models of PD have shed light on the understanding of this phenomenon, but the exploration of inflammation-driven models is necessary to better characterize this aspect of the disorder. The use of lipopolysaccharide (LPS) to induce a neuroinflammation-mediated neuronal loss is useful to induce reliable elimination of dopaminergic neurons. Nevertheless, how this model parallels the PD-like neuroinflammation is uncertain. In the present work, we used the direct LPS injection as a model inductor to eliminate dopaminergic neurons of the substantia nigra pars compacta (SNpc) in rats and reevaluated the inflammatory reaction. High-resolution 3D histological examination revealed that, although LPS induced a reliable elimination of SNpc dopaminergic neurons, it also generated a massive inflammatory response. This inflammation-mediated injury was characterized by corralling, a damaged parenchyma occupied by a vast population of lesion-associated microglia and macrophages (LAMMs) undertaking wound compaction and scar formation, surrounded by highly reactive astrocytes. LAMMs tiled the entire lesion and engaged in long-standing phagocytic activity to resolve the injury. Additionally, modeling LPS inflammation in a cell culture system helped to understand the role of phagocytosis and cytotoxicity in the initial phases of dopaminergic degeneration and indicated that LAMM-mediated toxicity and phagocytosis coexist during LPS-mediated dopaminergic elimination. However, this type of severe inflammatory-mediated injury, and subsequent resolution appear to be different from the ageing-related PD scenario where the architectural structure of the parenchyma is mostly preserved. Thus, the necessity to explore new experimental models to properly mimic the inflammatory compound observed in PD degeneration.
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Full text: 1 Collection: 01-internacional Database: MEDLINE Main subject: Parkinson Disease / Microglia Type of study: Prognostic_studies / Risk_factors_studies Limits: Animals Language: En Journal: J Neuroimmunol Year: 2022 Document type: Article Affiliation country: Mexico Country of publication: Netherlands

Full text: 1 Collection: 01-internacional Database: MEDLINE Main subject: Parkinson Disease / Microglia Type of study: Prognostic_studies / Risk_factors_studies Limits: Animals Language: En Journal: J Neuroimmunol Year: 2022 Document type: Article Affiliation country: Mexico Country of publication: Netherlands