Document Detail


Quantitative analysis of cellular inflammation after traumatic spinal cord injury: evidence for a multiphasic inflammatory response in the acute to chronic environment.
MedLine Citation:
PMID:  20085927     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Traumatic injury to the central nervous system results in the disruption of the blood brain/spinal barrier, followed by the invasion of cells and other components of the immune system that can aggravate injury and affect subsequent repair and regeneration. Although studies of chronic neuroinflammation in the injured spinal cord of animals are clinically relevant to most patients living with traumatic injury to the brain or spinal cord, very little is known about chronic neuroinflammation, though several studies have tested the role of neuroinflammation in the acute period after injury. The present study characterizes a novel cell preparation method that assesses, quickly and effectively, the changes in the principal immune cell types by flow cytometry in the injured spinal cord, daily for the first 10 days and periodically up to 180 days after spinal cord injury. These data quantitatively demonstrate a novel time-dependent multiphasic response of cellular inflammation in the spinal cord after spinal cord injury and are verified by quantitative stereology of immunolabelled spinal cord sections at selected time points. The early phase of cellular inflammation is comprised principally of neutrophils (peaking 1 day post-injury), macrophages/microglia (peaking 7 days post-injury) and T cells (peaking 9 days post-injury). The late phase of cellular inflammation was detected after 14 days post-injury, peaked after 60 days post-injury and remained detectable throughout 180 days post-injury for all three cell types. Furthermore, the late phase of cellular inflammation (14-180 days post-injury) did not coincide with either further improvements, or new decrements, in open-field locomotor function after spinal cord injury. However, blockade of chemoattractant C5a-mediated inflammation after 14 days post-injury reduced locomotor recovery and myelination in the injured spinal cord, suggesting that the late inflammatory response serves a reparative function. Together, these data provide new insight into cellular inflammation of spinal cord injury and identify a surprising and extended multiphasic response of cellular inflammation. Understanding the role of this multiphasic response in the pathophysiology of spinal cord injury could be critical for the design and implementation of rational therapeutic treatment strategies, including both cell-based and pharmacological interventions.
Authors:
Kevin D Beck; Hal X Nguyen; Manuel D Galvan; Desirée L Salazar; Trent M Woodruff; Aileen J Anderson
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Publication Detail:
Type:  Comparative Study; Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.     Date:  2010-01-19
Journal Detail:
Title:  Brain : a journal of neurology     Volume:  133     ISSN:  1460-2156     ISO Abbreviation:  Brain     Publication Date:  2010 Feb 
Date Detail:
Created Date:  2010-02-17     Completed Date:  2010-03-16     Revised Date:  2013-03-14    
Medline Journal Info:
Nlm Unique ID:  0372537     Medline TA:  Brain     Country:  England    
Other Details:
Languages:  eng     Pagination:  433-47     Citation Subset:  AIM; IM    
Affiliation:
Anatomy and Neurobiology, University of California, Irvine, CA 92697-4292, USA.
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MeSH Terms
Descriptor/Qualifier:
Acute Disease
Animals
Chronic Disease
Evaluation Studies as Topic*
Female
Inflammation / metabolism,  pathology
Inflammation Mediators / antagonists & inhibitors,  physiology*
Macrophages / drug effects,  pathology
Neutrophils / drug effects,  pathology
Peptides, Cyclic / pharmacology
Rats
Rats, Sprague-Dawley
Receptor, Anaphylatoxin C5a / antagonists & inhibitors,  physiology
Spinal Cord Injuries / metabolism,  pathology*
T-Lymphocytes / drug effects,  pathology
Thoracic Vertebrae / metabolism,  pathology*
Time Factors
Grant Support
ID/Acronym/Agency:
R01 NS43428-01/NS/NINDS NIH HHS; T32 NS007444/NS/NINDS NIH HHS
Chemical
Reg. No./Substance:
0/Inflammation Mediators; 0/Peptides, Cyclic; 0/Receptor, Anaphylatoxin C5a; 0/hydrocinnamate-cyclo(ornithyl-prolyl-cyclohexylalanyl-tryptophyl-arginyl)
Comments/Corrections

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