PMID- 11486101
OWN - NLM
STAT- MEDLINE
DCOM- 20010830
LR  - 20220317
IS  - 1524-4628 (Electronic)
IS  - 0039-2499 (Linking)
VI  - 32
IP  - 8
DP  - 2001 Aug
TI  - Evolution of cerebral tumor necrosis factor-alpha production during human 
      ischemic stroke.
PG  - 1750-8
AB  - BACKGROUND AND PURPOSE: Tumor necrosis factor-alpha (TNF-alpha) is detected in 
      ischemic brain cells in experimental animal models and is believed to play an 
      important role in apoptosis. However, the natural expression of TNF-alpha during 
      human stroke is not known. METHODS: We examined TNF-alpha immunohistochemistry 
      and terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling (TUNEL) 
      in brain samples of stroke victims (n=16) after variable survival (15 hours to 18 
      days). Systemic TNF-alpha content from a separate cohort including severe or 
      lethal stroke cases (n=26) was also assayed. RESULTS: Neuronal TNF-alpha was 
      demonstrated from 0.6 to 5.4 days after the onset of stroke symptoms, peaking 
      bilaterally during days 2 and 3. Bilateral glial TNF-alpha immunoreactivity was 
      detected during the acute phase, with the astrocytic TNF-alpha expression 
      dominating in later phases and persisting contralaterally to the infarct in more 
      matured phases (17 to 18 days). Invading inflammatory cells were TNF-alpha 
      immunopositive beginning on the third day. Besides, vascular wall structures 
      showed immunoreactivity sporadically. TNF-alpha levels were mostly nondetectable 
      in peripheral blood. TUNEL labeling and TNF-alpha staining overlapped, although 
      not completely, during the first days. CONCLUSIONS: The data support the 
      hypothesis that TNF-alpha may be involved both in the acute propagation of 
      inflammatory processes and cell death and possibly in the more delayed 
      reconstitutive processes of human ischemic stroke.
FAU - Sairanen, T
AU  - Sairanen T
AD  - Department of Clinical Neurosciences, Helsinki University Central Hospital, 
      University of Western Ontario, London, Ontario, Canada.
FAU - Carpen, O
AU  - Carpen O
FAU - Karjalainen-Lindsberg, M L
AU  - Karjalainen-Lindsberg ML
FAU - Paetau, A
AU  - Paetau A
FAU - Turpeinen, U
AU  - Turpeinen U
FAU - Kaste, M
AU  - Kaste M
FAU - Lindsberg, P J
AU  - Lindsberg PJ
LA  - eng
PT  - Journal Article
PL  - United States
TA  - Stroke
JT  - Stroke
JID - 0235266
RN  - 0 (Tumor Necrosis Factor-alpha)
SB  - IM
MH  - Adult
MH  - Aged
MH  - Aged, 80 and over
MH  - Apoptosis
MH  - Brain/*metabolism/pathology
MH  - Brain Ischemia/complications/*metabolism/pathology
MH  - Disease Progression
MH  - Female
MH  - Fluorescence
MH  - Humans
MH  - Immunohistochemistry
MH  - In Situ Nick-End Labeling
MH  - Male
MH  - Microcirculation/metabolism/pathology
MH  - Middle Aged
MH  - Neuroglia/metabolism/pathology
MH  - Neurons/metabolism/pathology
MH  - Phagocytes/metabolism/pathology
MH  - Stroke/complications/*metabolism/pathology
MH  - Tumor Necrosis Factor-alpha/*metabolism
EDAT- 2001/08/04 10:00
MHDA- 2001/08/31 10:01
CRDT- 2001/08/04 10:00
PHST- 2001/08/04 10:00 [pubmed]
PHST- 2001/08/31 10:01 [medline]
PHST- 2001/08/04 10:00 [entrez]
AID - 10.1161/01.str.32.8.1750 [doi]
PST - ppublish
SO  - Stroke. 2001 Aug;32(8):1750-8. doi: 10.1161/01.str.32.8.1750.