Prolonged and intense neuroinflammation after severe traumatic brain injury assessed by cerebral microdialysis with 300 kDa membranes
Cederberg, David LU ; Visse, Edward LU ; Marklund, Niklas LU
and Siesjö, Peter
LU
(2023)
In Journal of Neuroimmunology
377.
- Abstract
Background: A neuroinflammatory response that may lead to edema and secondary brain damage is elicited in severe traumatic brain injury (TBI). Previous studies using microdialysis (MD) membranes with 100 k Dalton (kDa) cut-off found a transient intracerebral release of cytokines and chemokines without significant correlations to clinical course, intracranial pressure (ICP) or metabolites. In this study, a (300 kDa) MD probe was used to measure the levels of cytokines and chemokines in relation to ICP and metabolites. Methods: Seven patients with severe TBI received 2 MD catheters. In four patients sufficient dialysate could be retrieved for analysis from both catheters. MD samples were analyzed bedside, then frozen and analyzed for... (More)
Background: A neuroinflammatory response that may lead to edema and secondary brain damage is elicited in severe traumatic brain injury (TBI). Previous studies using microdialysis (MD) membranes with 100 k Dalton (kDa) cut-off found a transient intracerebral release of cytokines and chemokines without significant correlations to clinical course, intracranial pressure (ICP) or metabolites. In this study, a (300 kDa) MD probe was used to measure the levels of cytokines and chemokines in relation to ICP and metabolites. Methods: Seven patients with severe TBI received 2 MD catheters. In four patients sufficient dialysate could be retrieved for analysis from both catheters. MD samples were analyzed bedside, then frozen and analyzed for chemokines and cytokines using a multiplex assay (Mesoscale Discovery). Results: MD sampling was performed from 9 to 350 h. In total, 17 chemokines and cytokines were detected. Of these, IL-6, IL-8, IP-10, MCP-1 and MIP-1β were consistently elevated, and investigated further in relation to metabolites, and ICP. Levels of chemokines and cytokines were higher than previously reported from TBI patients, and partially higher than those reported in patients with cytokine release syndrome. There were no significant differences between the two catheters regarding cytokine/chemokine concentrations, except for IL-6 which was higher in the peri-contusional area. No correlation with metabolites and ICP was observed. No significant increase or decline of chemokine or cytokine secretion was observed during the study period. Conclusion: Our data suggest that cytokine and chemokine levels reflect a perpetual, potent and pan-cerebebral inflammatory response that persists beyond 15 days following TBI.
(Less)
- author
- Cederberg, David
LU
; Visse, Edward
LU
; Marklund, Niklas
LU
and Siesjö, Peter
LU
- organization
- publishing date
- 2023-04-15
- type
- Contribution to journal
- publication status
- published
- subject
- keywords
- Brain injuries, Brain metabolism, Microdialysis, Neuroinflammation, Traumatic / pathology
- in
- Journal of Neuroimmunology
- volume
- 377
- article number
- 578020
- publisher
- Elsevier
- external identifiers
-
- scopus:85150062916
- pmid:36931209
- ISSN
- 0165-5728
- DOI
- 10.1016/j.jneuroim.2023.578020
- language
- English
- LU publication?
- yes
- id
- 80af404e-f950-44b6-bdf6-61bcceeaf1ab
- date added to LUP
- 2023-04-24 12:21:50
- date last changed
- 2024-06-16 04:44:51
@article{80af404e-f950-44b6-bdf6-61bcceeaf1ab,
abstract = {{<p>Background: A neuroinflammatory response that may lead to edema and secondary brain damage is elicited in severe traumatic brain injury (TBI). Previous studies using microdialysis (MD) membranes with 100 k Dalton (kDa) cut-off found a transient intracerebral release of cytokines and chemokines without significant correlations to clinical course, intracranial pressure (ICP) or metabolites. In this study, a (300 kDa) MD probe was used to measure the levels of cytokines and chemokines in relation to ICP and metabolites. Methods: Seven patients with severe TBI received 2 MD catheters. In four patients sufficient dialysate could be retrieved for analysis from both catheters. MD samples were analyzed bedside, then frozen and analyzed for chemokines and cytokines using a multiplex assay (Mesoscale Discovery). Results: MD sampling was performed from 9 to 350 h. In total, 17 chemokines and cytokines were detected. Of these, IL-6, IL-8, IP-10, MCP-1 and MIP-1β were consistently elevated, and investigated further in relation to metabolites, and ICP. Levels of chemokines and cytokines were higher than previously reported from TBI patients, and partially higher than those reported in patients with cytokine release syndrome. There were no significant differences between the two catheters regarding cytokine/chemokine concentrations, except for IL-6 which was higher in the peri-contusional area. No correlation with metabolites and ICP was observed. No significant increase or decline of chemokine or cytokine secretion was observed during the study period. Conclusion: Our data suggest that cytokine and chemokine levels reflect a perpetual, potent and pan-cerebebral inflammatory response that persists beyond 15 days following TBI.</p>}},
author = {{Cederberg, David and Visse, Edward and Marklund, Niklas and Siesjö, Peter}},
issn = {{0165-5728}},
keywords = {{Brain injuries; Brain metabolism; Microdialysis; Neuroinflammation; Traumatic / pathology}},
language = {{eng}},
month = {{04}},
publisher = {{Elsevier}},
series = {{Journal of Neuroimmunology}},
title = {{Prolonged and intense neuroinflammation after severe traumatic brain injury assessed by cerebral microdialysis with 300 kDa membranes}},
url = {{http://dx.doi.org/10.1016/j.jneuroim.2023.578020}},
doi = {{10.1016/j.jneuroim.2023.578020}},
volume = {{377}},
year = {{2023}},
}