Chemokine detection in the cerebral tissue of patients with posttraumatic brain contusions.
OBJECTIVE
The clinical outcome of patients with severe head injuries is still critically dependent on their secondary injuries. Although hypoxia and hypotension appear to mediate a substantial proportion of secondary injuries, many studies associate secondary brain injury with neuroinflammatory responses. Chemokines have been detected in the cerebrospinal fluid but not in the brain tissue of patients with head trauma. This study was performed to determine if chemokines were expressed in pericontusional brain tissue in patients with moderate or severe head trauma who underwent surgical evacuation of their brain contusions.


METHODS
Twelve patients with posttraumatic cerebral contusion requiring a surgical evacuation were studied. A 20- to 40-mg sample of white matter was removed from the surgical cavity in the pericontusional area. Two patients undergoing elective surgery for clip ligation of an unruptured aneurysm were used as controls. The median interval from trauma to biopsy procedure was 44 hours (range 3-360 hours). Total RNA was isolated from these samples and a ribonuclease protection assay was performed to measure the mRNA levels of several chemokines: CCL2, CCL3, CCL4, CCL5, CXCL8, CXCL10, and XCL1.


RESULTS
The CCL2, a monocyte chemoattractant produced by activated astrocytes, was the most strongly expressed chemokine, followed by CXCL8, CCL3, and CCL4. The chemokines CXCL10 and CCL5 were expressed at very low levels, and XCL1 was not detected.


CONCLUSIONS
Chemokine activation occurs early after moderate or severe head trauma and is maintained for several days after trauma. This event may contribute to neuroinflammatory exacerbation of posttraumatic brain damage in the pericontusional brain tissue.
Stefini
Roberto
R
Department of Neurosurgery, University of Brescia, Italy.
Catenacci
Emanuela
E
Piva
Simone
S
Sozzani
Silvano
S
Valerio
Alessandra
A
Bergomi
Riccardo
R
Cenzato
Marco
M
Mortini
Pietro
P
Latronico
Nicola
N
D001923:Brain Chemistry; D001930:Brain Injuries / Q000378:metabolism*; D018932:Chemokine CCL2 / Q000032:analysis; D054405:Chemokine CCL3 / Q000032:analysis; D054407:Chemokine CCL4 / Q000032:analysis; D018946:Chemokine CCL5 / Q000032:analysis; D054412:Chemokine CCL8 / Q000032:analysis; D018925:Chemokines / Q000032:analysis*; D005260:Female; D006801:Humans; D008297:Male; D008875:Middle Aged; D012333:RNA, Messenger / Q000032:analysis
D018932:Chemokine CCL2; D054405:Chemokine CCL3; D054407:Chemokine CCL4; D018946:Chemokine CCL5; D054412:Chemokine CCL8; D018925:Chemokines; D012333:RNA, Messenger