PMID- 17212701
OWN - NLM
STAT- MEDLINE
DCOM- 20070410
LR  - 20220311
IS  - 0022-3042 (Print)
IS  - 1471-4159 (Electronic)
IS  - 0022-3042 (Linking)
VI  - 100
IP  - 4
DP  - 2007 Feb
TI  - Macrophages are comprised of resident brain microglia not infiltrating peripheral 
      monocytes acutely after neonatal stroke.
PG  - 893-904
AB  - Macrophages can be both beneficial and detrimental after CNS injury. We 
      previously showed rapid accumulation of macrophages in injured immature brain 
      acutely after ischemia-reperfusion. To determine whether these macrophages are 
      microglia or invading monocytes, we subjected post-natal day 7 (P7) rats to 
      transient 3 h middle cerebral artery (MCA) occlusion and used flow cytometry at 
      24 and 48 h post-reperfusion to distinguish invading monocytes (CD45high/CD11b+) 
      from microglia (CD45low/medium/CD11b+). Inflammatory cytokines and chemokines 
      were determined in plasma, injured and contralateral tissue 1-24 h 
      post-reperfusion using ELISA-based cytokine multiplex assays. At 24 h, the number 
      of CD45+/CD11b+ cells increased 3-fold in injured compared to uninjured brain 
      tissue and CD45 expression shifted from low to medium with less than 10% of the 
      population expressing CD45high. MCA occlusion induced rapid and transient 
      asynchronous increases in the pro-inflammatory cytokine IL-beta and chemokines 
      cytokine-induced neutrophil chemoattractant protein 1 (CINC-1) and 
      monocyte-chemoattractant protein 1 (MCP-1), first in systemic circulation and 
      then in injured brain. Double immunofluorescence with cell-type specific markers 
      showed that multiple cell types in the injured brain produce MCP-1. Our findings 
      show that despite profound increases in MCP-1 in injured regions, monocyte 
      infiltration is low and the majority of macrophages in acutely injured regions 
      are microglia.
FAU - Denker, Sheryl P
AU  - Denker SP
AD  - Department of Neurology, University of California San Francisco, San Francisco, 
      CA 94143-0663, USA.
FAU - Ji, Shaoquan
AU  - Ji S
FAU - Dingman, Andra
AU  - Dingman A
FAU - Lee, Sarah Y
AU  - Lee SY
FAU - Derugin, Nikita
AU  - Derugin N
FAU - Wendland, Michael F
AU  - Wendland MF
FAU - Vexler, Zinaida S
AU  - Vexler ZS
LA  - eng
GR  - R01 NS044025/NS/NINDS NIH HHS/United States
GR  - R01 NS044025-03/NS/NINDS NIH HHS/United States
GR  - R01 NS044025-04/NS/NINDS NIH HHS/United States
GR  - NS44025/NS/NINDS NIH HHS/United States
PT  - Journal Article
PT  - Research Support, N.I.H., Extramural
DEP - 20061222
PL  - England
TA  - J Neurochem
JT  - Journal of neurochemistry
JID - 2985190R
RN  - 0 (CD11b Antigen)
RN  - 0 (Chemokines)
RN  - 0 (Cytokines)
RN  - 0 (Glial Fibrillary Acidic Protein)
RN  - 0 (Lectins)
RN  - EC 3.1.3.48 (Leukocyte Common Antigens)
SB  - IM
MH  - Analysis of Variance
MH  - Animals
MH  - Animals, Newborn
MH  - CD11b Antigen/metabolism
MH  - Chemokines/metabolism
MH  - Cytokines/metabolism
MH  - Female
MH  - Flow Cytometry
MH  - Glial Fibrillary Acidic Protein/metabolism
MH  - Immunohistochemistry
MH  - Lectins/metabolism
MH  - Leukocyte Common Antigens/metabolism
MH  - Macrophage Activation/physiology
MH  - Macrophages/*physiology
MH  - Microglia/metabolism/*physiology
MH  - Monocytes/metabolism/*physiology
MH  - Rats
MH  - Rats, Sprague-Dawley
MH  - Reperfusion Injury
MH  - Stroke/*pathology/*physiopathology
MH  - Time Factors
PMC - PMC2262099
MID - NIHMS39283
EDAT- 2007/01/11 09:00
MHDA- 2007/04/11 09:00
PMCR- 2008/03/03
CRDT- 2007/01/11 09:00
PHST- 2007/01/11 09:00 [pubmed]
PHST- 2007/04/11 09:00 [medline]
PHST- 2007/01/11 09:00 [entrez]
PHST- 2008/03/03 00:00 [pmc-release]
AID - JNC4162 [pii]
AID - 10.1111/j.1471-4159.2006.04162.x [doi]
PST - ppublish
SO  - J Neurochem. 2007 Feb;100(4):893-904. doi: 10.1111/j.1471-4159.2006.04162.x. Epub 
      2006 Dec 22.