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Review Article

Microglia and astroglia: the role of

neuroinflammation in lead toxicity and neuronal

injury in the brain

3
1,2
3
1
Jin‑Tao Liu , Mo‑Han Dong , Jie‑Qiong Zhang , Ya Bai , Fang Kuang , Liang‑Wei Chen 1
4
1 Institute of Neurosciences, The Fourth Military Medical University, Xi’an 710032, Shaanxi, China.
2 Department of Neurosurgery, Tangdu Hospital, The Fourth Military Medical University, Xi’an 710032, Shaanxi, China.
3 School of Military Preventive Medicine, The Fourth Military Medical University, Xi’an 710032, Shaanxi, China.
4 Department of Neurology, Xijing Hospital, The Fourth Military Medical University, Xi’an 710032, Shaanxi, China.
ABSTRA CT
2 +
Lead (Pb ), a ubiquitous environmental toxicant, may widely affect the function of many organs or systems of human beings,
especially the brain. Although lead is believed to transport into the brain through the blood‑brain barrier (BBB) and cause direct
neuronal injury, growing data have shown that lead exposure could induce brain dysfunction by triggering microglial and astroglial
activation, pro‑inflammatory cytokine production and inflammatory response, generation of reactive oxygen species and oxidative
stress, and finally result in BBB dysfunction and neuronal damage. This review summarizes recent studies regarding microglial and
astroglial reaction, neuroinflammation, and neuronal death in the brain following lead insult, suggesting that reactive glial cells may
represent a potential target for manipulation of lead‑induced neuroinflammatory injury of the brain.

Key words: Astroglia, brain, lead toxicity, microglia, neuroinflammation

INTRODUCTION enhance production of amyloid protein. [6-13] Lead can
also bind to key metabolic enzymes such as pyruvate
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Lead (Pb ) is a widely distributed heavy metal and kinase, induce reactive oxygen species (ROS), impede
environmental toxicant, and overexposure to lead due the supply of energy to neurons, and cause neuronal
to pollution or accident can impair the function of apoptosis. [14-17] Moreover, recent studies have shown a
the nervous system, especially learning and memory crucial involvement of microglial and astroglial cells in
abilities of developing brains during childhood. [1-4] neuroinflammatory injury induced by lead exposure. [10,11]
Epidemiologic data indicate that learning impairment Microglia and astrocytes are two major types of glial
may be caused by moderate lead exposure in young cells involved in the regulation of the immune response
individuals. [2,3] This impairment is largely related to to pathological processes in the brain. [18] Functional
neuronal injury caused by lead toxicity, but the detailed activation of microglia and astrocytes and the resulting
mechanism by which lead exposure induces neuronal neuroinflammation are associated with infection,
injury, neuronal death, and brain dysfunction still autoimmunity, and pathogenesis of neurodegenerative
remains elusive. [4,5] Several studies have indicated that diseases. In response to lead exposure, microglia and
lead exposure may interfere with calcium signaling, astrocytes can increase the production and release
suppress neurogenesis and neuronal differentiation, of inflammatory cytokines, enhance ROS generation,
inhibit formation of long-term potentiation (LTP), impede antioxidant activity, and result in neuronal
influence secretion of neurotransmitters, and even injury or neuronal loss in the brain or other parts of the
central nervous system (CNS). [10,11,19-22]
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Quick Response Code: MICROGLIAL ACTIVATION, PRO‑INFLAMMATORY
Website:
www.nnjournal.net CYTOKINES, AND NEUROINFLAMMATION

DOI: It is generally regarded that microglial cells are
10.4103/2347-8659.156980 derived from blood monocytes that reset in the CNS
during embryonic development and are functionally

Corresponding Author: Dr. Liang‑Wei Chen, Institute of Neurosciences, The Fourth Military Medical University, No. 169
Changle West Road, Xi’an 710032, Shaanxi, China. E‑mail: lwchen@fmmu.edu.cn

PB Neuroimmunol Neuroinflammation | Volume 2 | Issue 3 | July 15, 2015 Neuroimmunol Neuroinflammation | Volume 2 | Issue 3 | July 15, 2015 131