PMID- 11284554
OWN - NLM
STAT- MEDLINE
DCOM- 20010809
LR  - 20220330
IS  - 0897-7151 (Print)
IS  - 0897-7151 (Linking)
VI  - 18
IP  - 3
DP  - 2001 Mar
TI  - Astrocytes produce and release interleukin-1, interleukin-6, tumor necrosis 
      factor alpha and interferon-gamma following traumatic and metabolic injury.
PG  - 351-9
AB  - The brain is no longer considered immune-privileged due to its capability of 
      producing cytokines in response to neurotrauma; however, the cellular sources of 
      cytokines have not been defined. This study focused on the production of four 
      inflammatory cytokines, interleukin-1 (IL-1alpha), interleukin-6 (IL-6), tumor 
      necrosis factor alpha (TNFalpha), and interferon gamma (IFN-gamma) in primary 
      culture of astrocytes under two different injury models which simulated in vivo 
      mechanical trauma (scratch injury) and ischemia. Results demonstrated that 
      astrocytes after scratch injury were positively immunostained with IL-1alpha, 
      IL-6, and TNFalpha. A slot-blot study of culture media showed that the release of 
      IL-1alpha, IL-6, TNFalpha, and IFN-gamma by astrocytes subsequent to scratch and 
      ischemic injury reached approximately twice the control values. The temporal 
      expression of these cytokines was different for the two models. All four 
      cytokines began to increase 1 h postscratch and remained at high levels 
      throughout the experiment. In the ischemic model, however, the increase of 
      cytokine expression was delayed until 4-8 h of ischemia, when sharp increases 
      were seen in all four cytokines. In this culture system, the exogenous influence 
      of blood-borne factors and leukocytes, which occur with in vivo trauma and 
      ischemia, was eliminated. Accordingly, the cytokines detected in the culture 
      media were derived from astrocytes. This study provides the first evidence that 
      astrocytes, without the influence from other cell types, can produce and release 
      cytokines following mechanical and ischemic injury.
FAU - Lau, L T
AU  - Lau LT
AD  - Department of Biology, The Hong Kong University of Science and Technology, Clear 
      Water Bay, Kowloon, China.
FAU - Yu, A C
AU  - Yu AC
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - United States
TA  - J Neurotrauma
JT  - Journal of neurotrauma
JID - 8811626
RN  - 0 (Interleukin-1)
RN  - 0 (Interleukin-6)
RN  - 0 (Tumor Necrosis Factor-alpha)
RN  - 82115-62-6 (Interferon-gamma)
SB  - IM
MH  - Animals
MH  - Animals, Newborn
MH  - Astrocytes/*metabolism
MH  - Cell Hypoxia/physiology
MH  - Cells, Cultured
MH  - Cerebral Cortex/cytology/injuries
MH  - Interferon-gamma/*metabolism
MH  - Interleukin-1/*metabolism
MH  - Interleukin-6/*metabolism
MH  - Mice
MH  - Tumor Necrosis Factor-alpha/*metabolism
EDAT- 2001/04/04 10:00
MHDA- 2001/08/15 10:01
CRDT- 2001/04/04 10:00
PHST- 2001/04/04 10:00 [pubmed]
PHST- 2001/08/15 10:01 [medline]
PHST- 2001/04/04 10:00 [entrez]
AID - 10.1089/08977150151071035 [doi]
PST - ppublish
SO  - J Neurotrauma. 2001 Mar;18(3):351-9. doi: 10.1089/08977150151071035.