Abstract
OBJECTIVE: Posttraumatic temperature manipulations have been reported to significantly influence the inflammatory response to traumatic brain injury (TBI). The purpose of this study was to determine the temporal and regional profiles of messenger ribonucleic acid (mRNA) expression and protein levels for the proinflammatory cytokine interleukin-1β (IL-1β, after moderate or severe TBI. The effects of posttraumatic hypothermia (33°C) or hyperthermia (39.5°C) on these consequences of TBI were then determined. METHODS: Male Sprague-Dawley rats underwent fluid-percussion brain injury. In the first phase of the study, rats were killed 15 minutes or 1, 3, or 24 hours after moderate TBI (1.8-2.2 atmospheres), for reverse transcription-polymerase chain reaction analysis. Other groups of rats were killed 1, 3, 24, or 72 hours after moderate or severe TBI (2.4-2.7 atmospheres), for protein analysis. In the second phase, rats underwent moderate fluid-percussion brain injury, followed immediately by 3 hours of posttraumatic normothermia (37°C), hyperthermia (39.5°C), or hypothermia (33°C), and were then killed, for analyses of protein levels and mRNA expression. Brain samples, including cerebral cortex, hippocampus, thalamus, and cerebellum, were dissected and stored at -80°C until analyzed. RESULTS: The findings indicated that mRNA levels were increased (P < 0.05) as early as 1 hour after TBI and remained elevated up to 3 hours after moderate TBI. Although both moderate and severe TBI induced increased levels of IL-1β (P < 0.05), increased protein levels were also noted in remote brain structures after severe TBI. Posttraumatic hypothermia attenuated IL-1β protein levels, compared with normothermia (P < 0.05), although the levels remained elevated in comparison with sham values. In contrast, hyperthermia had no significant effect on IL-1β levels, compared with normothermic values. Posttraumatic temperature manipulations had no significant effect on IL-1β mRNA levels. CONCLUSION: Injury severity determines the degree of IL-1β protein level elevation after TBI. The effects of posttraumatic hypothermia on IL-1β protein levels (an important mediator of neurodegeneration after TBI) may partly explain the established effects of posttraumatic temperature manipulations on inflammatory processes after TBI.
| Original language | English |
|---|---|
| Pages (from-to) | 195-203 |
| Number of pages | 9 |
| Journal | Neurosurgery |
| Volume | 51 |
| Issue number | 1 |
| DOIs | |
| State | Published - Jul 1 2002 |
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Keywords
- Hyperthermia
- Hypothermia
- Inflammation and secondary injury
- Interleukin-1β
- Traumatic brain injury
ASJC Scopus subject areas
- Clinical Neurology
- Surgery
Cite this
Interleukin-1β messenger ribonucleic acid and protein levels after fluid-percussion brain injury in rats : Importance of injury severity and brain temperature. / Kinoshita, Kosaku; Chatzipanteli, Katina; Vitarbo, Elizabeth; Truettner, Jessie S.; Alonso, Ofelia F.; Dalton Dietrich, W.; Selman, Warren R.; Lee, Stefan M.; Kelly, Daniel F.
In: Neurosurgery, Vol. 51, No. 1, 01.07.2002, p. 195-203.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - Interleukin-1β messenger ribonucleic acid and protein levels after fluid-percussion brain injury in rats
T2 - Importance of injury severity and brain temperature
AU - Kinoshita, Kosaku
AU - Chatzipanteli, Katina
AU - Vitarbo, Elizabeth
AU - Truettner, Jessie S.
AU - Alonso, Ofelia F.
AU - Dalton Dietrich, W.
AU - Selman, Warren R.
AU - Lee, Stefan M.
AU - Kelly, Daniel F.
PY - 2002/7/1
Y1 - 2002/7/1
N2 - OBJECTIVE: Posttraumatic temperature manipulations have been reported to significantly influence the inflammatory response to traumatic brain injury (TBI). The purpose of this study was to determine the temporal and regional profiles of messenger ribonucleic acid (mRNA) expression and protein levels for the proinflammatory cytokine interleukin-1β (IL-1β, after moderate or severe TBI. The effects of posttraumatic hypothermia (33°C) or hyperthermia (39.5°C) on these consequences of TBI were then determined. METHODS: Male Sprague-Dawley rats underwent fluid-percussion brain injury. In the first phase of the study, rats were killed 15 minutes or 1, 3, or 24 hours after moderate TBI (1.8-2.2 atmospheres), for reverse transcription-polymerase chain reaction analysis. Other groups of rats were killed 1, 3, 24, or 72 hours after moderate or severe TBI (2.4-2.7 atmospheres), for protein analysis. In the second phase, rats underwent moderate fluid-percussion brain injury, followed immediately by 3 hours of posttraumatic normothermia (37°C), hyperthermia (39.5°C), or hypothermia (33°C), and were then killed, for analyses of protein levels and mRNA expression. Brain samples, including cerebral cortex, hippocampus, thalamus, and cerebellum, were dissected and stored at -80°C until analyzed. RESULTS: The findings indicated that mRNA levels were increased (P < 0.05) as early as 1 hour after TBI and remained elevated up to 3 hours after moderate TBI. Although both moderate and severe TBI induced increased levels of IL-1β (P < 0.05), increased protein levels were also noted in remote brain structures after severe TBI. Posttraumatic hypothermia attenuated IL-1β protein levels, compared with normothermia (P < 0.05), although the levels remained elevated in comparison with sham values. In contrast, hyperthermia had no significant effect on IL-1β levels, compared with normothermic values. Posttraumatic temperature manipulations had no significant effect on IL-1β mRNA levels. CONCLUSION: Injury severity determines the degree of IL-1β protein level elevation after TBI. The effects of posttraumatic hypothermia on IL-1β protein levels (an important mediator of neurodegeneration after TBI) may partly explain the established effects of posttraumatic temperature manipulations on inflammatory processes after TBI.
AB - OBJECTIVE: Posttraumatic temperature manipulations have been reported to significantly influence the inflammatory response to traumatic brain injury (TBI). The purpose of this study was to determine the temporal and regional profiles of messenger ribonucleic acid (mRNA) expression and protein levels for the proinflammatory cytokine interleukin-1β (IL-1β, after moderate or severe TBI. The effects of posttraumatic hypothermia (33°C) or hyperthermia (39.5°C) on these consequences of TBI were then determined. METHODS: Male Sprague-Dawley rats underwent fluid-percussion brain injury. In the first phase of the study, rats were killed 15 minutes or 1, 3, or 24 hours after moderate TBI (1.8-2.2 atmospheres), for reverse transcription-polymerase chain reaction analysis. Other groups of rats were killed 1, 3, 24, or 72 hours after moderate or severe TBI (2.4-2.7 atmospheres), for protein analysis. In the second phase, rats underwent moderate fluid-percussion brain injury, followed immediately by 3 hours of posttraumatic normothermia (37°C), hyperthermia (39.5°C), or hypothermia (33°C), and were then killed, for analyses of protein levels and mRNA expression. Brain samples, including cerebral cortex, hippocampus, thalamus, and cerebellum, were dissected and stored at -80°C until analyzed. RESULTS: The findings indicated that mRNA levels were increased (P < 0.05) as early as 1 hour after TBI and remained elevated up to 3 hours after moderate TBI. Although both moderate and severe TBI induced increased levels of IL-1β (P < 0.05), increased protein levels were also noted in remote brain structures after severe TBI. Posttraumatic hypothermia attenuated IL-1β protein levels, compared with normothermia (P < 0.05), although the levels remained elevated in comparison with sham values. In contrast, hyperthermia had no significant effect on IL-1β levels, compared with normothermic values. Posttraumatic temperature manipulations had no significant effect on IL-1β mRNA levels. CONCLUSION: Injury severity determines the degree of IL-1β protein level elevation after TBI. The effects of posttraumatic hypothermia on IL-1β protein levels (an important mediator of neurodegeneration after TBI) may partly explain the established effects of posttraumatic temperature manipulations on inflammatory processes after TBI.
KW - Hyperthermia
KW - Hypothermia
KW - Inflammation and secondary injury
KW - Interleukin-1β
KW - Traumatic brain injury
UR - http://www.scopus.com/inward/record.url?scp=0036664602&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=0036664602&partnerID=8YFLogxK
U2 - 10.1097/00006123-200207000-00027
DO - 10.1097/00006123-200207000-00027
M3 - Article
C2 - 12182417
AN - SCOPUS:0036664602
VL - 51
SP - 195
EP - 203
JO - Neurosurgery
JF - Neurosurgery
SN - 0148-396X
IS - 1
ER -