Inflammatory Activation of Microglia and Astrocytes in Manganese Neurotoxicity

• Published in: Advances in neurobiology Vol. 18; pp. 159 - 181
• Main Authors: Tjalkens, Ronald B., Popichak, Katriana A., Kirkley, Kelly A.
• Format: Book Chapter Journal Article
• Language: English
• Published: Cham Springer International Publishing 2017
• Series: Advances in Neurobiology
• Subjects: Astrocytes - immunology; Astrocytes - metabolism; Astrogliosis; Brain - immunology; Brain - metabolism; Brain - physiopathology; Glial Fibrillary Acidic Protein; Glial fibrillary acidic protein (GFAP); Humans; Inflammation; Manganese Poisoning - immunology; Manganese Poisoning - metabolism; Manganese Poisoning - physiopathology; Manganism; Microglia - immunology; Microglia - metabolism; Neurons - metabolism; Neurotoxicity Syndromes - immunology; Neurotoxicity Syndromes - metabolism; Neurotoxicity Syndromes - physiopathology; Parkinsonian Disorders - immunology; Parkinsonian Disorders - metabolism; Parkinsonian Disorders - physiopathology; Parkinson’s disease (PD); Pattern recognition receptors (PRRs); Receptors, Pattern Recognition - metabolism; Signal Transduction; Astrogliosis; Glial fibrillary acidic protein (GFAP); Pattern recognition receptors (PRRs); Parkinson’s disease (PD); Manganism
• ISBN: 3319601881; 9783319601885
• ISSN: 2190-5215; 2190-5223
• DOI: 10.1007/978-3-319-60189-2_8

Neurotoxicity due to excessive exposure to manganese (Mn) has been described as early as 1837 (Couper, Br Ann Med Pharm Vital Stat Gen Sci 1:41–42, 1837). Extensive research over the past two decades has revealed that Mn-induced neurological injury involves complex pathophysiological signaling mechanisms between neurons and glial cells. Glial cells are an important target of Mn in the brain, both for sequestration of the metal, as well as for activating inflammatory signaling pathways that damage neurons through overproduction of numerous reactive oxygen and nitrogen species and inflammatory cytokines. Understanding how these pathways are regulated in glial cells during Mn exposure is critical to determining the mechanisms underlying permanent neurological dysfunction stemming from excess exposure. The subject of this review will be to delineate mechanisms by which Mn interacts with glial cells to perturb neuronal function, with a particular emphasis on neuroinflammation and neuroinflammatory signaling between distinct populations of glial cells.