PMID- 23651534
OWN - NLM
STAT- MEDLINE
DCOM- 20131105
LR  - 20220330
IS  - 1742-2094 (Electronic)
IS  - 1742-2094 (Linking)
VI  - 10
DP  - 2013 May 7
TI  - Acute and subacute IL-1beta administrations differentially modulate neuroimmune and 
      neurotrophic systems: possible implications for neuroprotection and 
      neurodegeneration.
PG  - 59
LID - 10.1186/1742-2094-10-59 [doi]
AB  - BACKGROUND: In Alzheimer's disease, stroke and brain injuries, activated 
      microglia can release proinflammatory cytokines, such as interleukin (IL)-1beta. 
      These cytokines may change astrocyte and neurotrophin functions, which influences 
      neuronal survival and induces apoptosis. However, the interaction between 
      neuroinflammation and neurotrophin functions in different brain conditions is 
      unknown. The present study hypothesized that acute and subacute elevated IL-1beta 
      differentially modulates glial and neurotrophin functions, which are related to 
      their role in neuroprotection and neurodegeneration. METHOD: Rats were i.c.v. 
      injected with saline or IL-1beta for 1 or 8 days and tested in a radial maze. mRNA 
      and protein expressions of glial cell markers, neurotrophins, neurotrophin 
      receptors, beta-amyloid precursor protein (APP) and the concentrations of pro- and 
      anti-inflammatory cytokines were measured in the hippocampus. RESULTS: When 
      compared to controls, memory deficits were found 4 days after IL-1 
      administrations, however the deficits were attenuated by IL-1 receptor antagonist 
      (RA). Subacute IL-1 administrations increased expressions of APP, microglial 
      active marker CD11b, and p75 neurotrophin receptor, and the concentration of 
      tumor necrosis factor (TNF)-alpha and IL-1beta, but decreased expressions of astrocyte 
      active marker glial fibrillary acidic protein (GFAP), brain-derived neurotrophic 
      factor (BDNF) and TrK B. By contrast, up-regulations of NGF, BDNF and TrK B 
      expressions were found after acute IL-1 administration, which are associated with 
      the increase in both glial marker expressions and IL-10 concentrations. However, 
      TrK A was down-regulated by acute and up-regulated by subacute IL-1 
      administrations. Subacute IL-1-induced changes in the glial activities, cytokine 
      concentrations and expressions of BDNF and p75 were reversed by IL-1RA treatment. 
      CONCLUSION: These results indicate that acute and subacute IL-1 administrations 
      induce different changes toward neuroprotection after acute IL-1 administrations 
      but neurodegeneration after subacute ones.
FAU - Song, Cai
AU  - Song C
AD  - Research Institute of Marine Drug and Nutrition, Guangdong Ocean University, 
      Zhanjiang, Guangdong, China. cai.song@dal.ca
FAU - Zhang, Ye
AU  - Zhang Y
FAU - Dong, Yilong
AU  - Dong Y
LA  - eng
GR  - Canadian Institutes of Health Research/Canada
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20130507
PL  - England
TA  - J Neuroinflammation
JT  - Journal of neuroinflammation
JID - 101222974
RN  - 0 (Amyloid beta-Protein Precursor)
RN  - 0 (Brain-Derived Neurotrophic Factor)
RN  - 0 (CD11b Antigen)
RN  - 0 (Cytokines)
RN  - 0 (Glial Fibrillary Acidic Protein)
RN  - 0 (Interleukin-1beta)
RN  - 0 (Nerve Growth Factors)
RN  - 0 (Neuroprotective Agents)
RN  - 0 (Receptor, Nerve Growth Factor)
RN  - EC 2.7.10.1 (Receptor, trkA)
RN  - EC 2.7.10.1 (Receptor, trkB)
SB  - IM
MH  - Amyloid beta-Protein Precursor/metabolism
MH  - Animals
MH  - Behavior, Animal/drug effects
MH  - Blotting, Western
MH  - Brain-Derived Neurotrophic Factor/metabolism
MH  - CD11b Antigen/metabolism
MH  - Cytokines/pharmacology
MH  - Data Interpretation, Statistical
MH  - Enzyme-Linked Immunosorbent Assay
MH  - Glial Fibrillary Acidic Protein/metabolism
MH  - Hippocampus/physiology
MH  - Injections, Intraventricular
MH  - Interleukin-1beta/*pharmacology
MH  - Male
MH  - Memory, Short-Term/drug effects
MH  - Nerve Degeneration/*pathology
MH  - Nerve Growth Factors/*metabolism
MH  - Nervous System/drug effects/*immunology
MH  - Neuroprotective Agents/*pharmacology
MH  - Polymerase Chain Reaction
MH  - Rats
MH  - Rats, Long-Evans
MH  - Receptor, Nerve Growth Factor/metabolism
MH  - Receptor, trkA/metabolism
MH  - Receptor, trkB/metabolism
PMC - PMC3656796
EDAT- 2013/05/09 06:00
MHDA- 2013/11/06 06:00
PMCR- 2013/05/07
CRDT- 2013/05/09 06:00
PHST- 2013/02/28 00:00 [received]
PHST- 2013/04/22 00:00 [accepted]
PHST- 2013/05/09 06:00 [entrez]
PHST- 2013/05/09 06:00 [pubmed]
PHST- 2013/11/06 06:00 [medline]
PHST- 2013/05/07 00:00 [pmc-release]
AID - 1742-2094-10-59 [pii]
AID - 10.1186/1742-2094-10-59 [doi]
PST - epublish
SO  - J Neuroinflammation. 2013 May 7;10:59. doi: 10.1186/1742-2094-10-59.