What are Microglia and their immune functions in the brain? Microglia are immune system cells that originate in bone marrow and migrate from blood to the brain acting as the first and main form of active immune defense in the central nervous system (CNS). They defend the brain and spinal cord, constantly excavating the CNS and attacking and engulfing infectious agents. In this process they release pro-inflammatory cytokines that can lead to inflammation of the brain and death of neurons. Their normal activity is the repair of damage caused by foreign insult (traumatic brain injury, toxins, microorganisms, viruses).  However, in the disease states associated with activation of the microglia they release cytokines, chemokines, hydrogen peroxide and nitrous oxide (latter two cause free radical formation).  The cytokines and chemokines attract lymphocytes, neutrophils and macrophages from the blood into the brain or spinal cord. In the activated state these compounds cause destruction of myelin and death of neurons.  I will only cover some of the disease states.  All the reader needs to perform is to enter entrez pubmed and search the National Library of Medicine.  

Macrophages, Cytokines and Chemokines in CNS Regulation and Pathology

Block ML, Calderon-Garciduenas L. 2009. Air pollution: Mechanisms of neuroinflammation and CNS Disease. Trends Neurosci 32:506-16.

D’Mello C, Le T, Swain MG. 2009. Cerebral microglia recruit monocytes into the brain in response to tumor necrosis factor α signaling during peripheral organ inflammation. Neurobiol Dis 29:2089-2102.

Laskin DL. 2009. Macrophages and inflammatory mediators in chemical toxicity: A battle of forces. Chem Res Toxicol 22:1376-85.

Neumann H, Kotter MR, Franklin RJM. 2009. Debris clearance by microglia: an essential link between degeneration and regeneration. Brain 132:288-295.

Cunningham C, Campion S, Lunnon K, Murray CL, et al. 2009. Systemic inflammation induces acute behavior and cognitive changes and accelerates neurodegenerative disease. Biol Psychiatry 65:304-12.

Miller AH, Maletic V, Raison CL. 2008. Inflammation and its discontents: The role of cytokines in the pathophysiology of major depression. Biol Psychiatry 65:732-41.

De Hass AH, van Weering HRJ, de Jong EK, Boddeke HWGM, Biber KPH. 2007 Neuronal chemokines: Versatile messengers in central nervous system interaction. Mol Neurobiol 36:137-52.

Abbadie C, Bhangoo S, De Koninck Y, Malcangio M, Melik-Parsadaniantz S, White FA 2009 Chemokines in pain mechanisms. Bran Res  60:125-34.

Callewaere C, Banisadr B, Rostene W, Melik-Parsadaniantz S 2007 Chemokines and chemokine receptors in the brain: Implication in neuroendocrine regulation. J Mol Endocrinol 38:355-63.

Liu B, Hong JS. 2002. Role of microglia in inflammation-mediated neurodegenerative diseases: Mechanisms and strategies for therapeutic intervention. J Pharmacol Exper Therap 304:1-7.

Alzheimer’s Disease: Alzheimer’s disease is characterized by the deposition of amyloid-β (Aβ) plaques in the brain parenchnyma and neurofibrillary tangles within neurons.  Its neurodegenerative conditons are characterized by chronic neuroinflammation. Currently, questions still arise as whether the inflammation is an underlying cause or a resulting condition of AD.  Nevertheless, it is important to recognize that chronic inflammation is present and therefore the disease is listed in this section of brain function and inflammation.  Contribution to of toxic exposure as either a cause or exacerbation of AD cannot be ruled out.