PMID- 24083053
OWN - NLM
STAT- PubMed-not-MEDLINE
DCOM- 20140624
LR  - 20211021
IS  - 2229-5097 (Print)
IS  - 2152-7806 (Electronic)
IS  - 2152-7806 (Linking)
VI  - 4
DP  - 2013 Sep 18
TI  - Immunology primer for neurosurgeons and neurologists part 2: Innate brain 
      immunity.
PG  - 118
LID - 10.4103/2152-7806.118349 [doi]
LID - 118
AB  - Over the past several decades we have learned a great deal about microglia and 
      innate brain immunity. While microglia are the principle innate immune cells, 
      other cell types also play a role, including invading macrophages, astrocytes, 
      neurons, and endothelial cells. The fastest reacting cell is the microglia and 
      despite its name, resting microglia (also called ramified microglia) are in fact 
      quite active. Motion photomicrographs demonstrate a constant movement of ramified 
      microglial foot processes, which appear to be testing the microenvironment for 
      dangerous alteration in extracellular fluid content. These foot processes, in 
      particular, interact with synapses and play a role in synaptic function. In event 
      of excitatory overactivity, these foot processes can strip selected synapses, 
      thus reducing activation states as a neuroprotective mechanism. They can also 
      clear extracellular glutamate so as to reduce the risk of excitotoxicity. 
      Microglia also appear to have a number of activation phenotypes, such as: (1) 
      phagocytic, (2) neuroprotective and growth promoting, or (3) primarily 
      neurodestructive. These innate immune cells can migrate a great distance under 
      pathological conditions and appear to have anatomic specificity, meaning they can 
      accumulate in specifically selected areas of the brain. There is some evidence 
      that there are several types of microglia. Macrophage infiltration into the 
      embryonic brain is the source of resident microglia and in adulthood macrophages 
      can infiltrate the brain and are for the most part pathologically 
      indistinguishable from resident microglia, but may react differently. Activation 
      itself does not imply a destructive phenotype and can be mostly neuroprotective 
      via phagocytosis of debris, neuron parts and dying cells and by the release of 
      neurotrophins such as nerve growth factor (NGF) and brain derived neurotrophic 
      factor (BDNF). Evidence is accumulating that microglia undergo dynamic 
      fluctuations in phenotype as the neuropathology evolves. For example, in the 
      early stages of neurotrauma and stroke, microglia play a mostly neuroprotective 
      role and only later switch to a neurodestructive mode. A great number of 
      biological systems alter microglia function, including neurohormones, 
      cannabinoids, other neurotransmitters, adenosine triphosphate (ATP), adenosine, 
      and corticosteroids. One can appreciate that with aging many of these systems are 
      altered by the aging process itself or by disease thus changing the sensitivity 
      of the innate immune system.
FAU - Blaylock, Russell L
AU  - Blaylock RL
AD  - Theoretical Neurosciences Research, LLC, Neurosurgeon (Ret), Ridgeland, MS.
LA  - eng
PT  - Journal Article
PT  - Review
DEP - 20130918
PL  - United States
TA  - Surg Neurol Int
JT  - Surgical neurology international
JID - 101535836
PMC - PMC3784951
OTO - NOTNLM
OT  - Immune surface receptors
OT  - immunoexcitotoxicity
OT  - innate immunity
OT  - microglia
OT  - microglial priming
EDAT- 2013/10/02 06:00
MHDA- 2013/10/02 06:01
PMCR- 2013/09/18
CRDT- 2013/10/02 06:00
PHST- 2013/06/17 00:00 [received]
PHST- 2013/06/18 00:00 [accepted]
PHST- 2013/10/02 06:00 [entrez]
PHST- 2013/10/02 06:00 [pubmed]
PHST- 2013/10/02 06:01 [medline]
PHST- 2013/09/18 00:00 [pmc-release]
AID - SNI-4-118 [pii]
AID - 10.4103/2152-7806.118349 [doi]
PST - epublish
SO  - Surg Neurol Int. 2013 Sep 18;4:118. doi: 10.4103/2152-7806.118349.