Biology Reference
In-Depth Information
Following brain injury, chemokines are rapidly released by activated resident
microglia and astroglial cells. Chemokine expression is regulated by cytokines such
as TNF and TGF-
[112,113]
. Studies over the past two decades, with both patients
and experimental models, have reported the release of several chemokines follow-
ing TBI (
Table 10.2
). The elevation of IL-8 (known by systemic nomenclature as
Table 10.2
Detection of Chemokine Production and Function in Rodents and Humans
Following Traumatic Brain Injury
Experimental
Approach
Human CSF, Serum,
or
Brain Tissue
Rodent Serum or
Brain Tissue
Gene Knockout or
Inhibition with Anti-
Sense Oligonucleotides
[
148
]
IL-8 (CXCL8)
[54]
[
147
]
[37]
[
149
]
[36]
, [148]
[39]
[117]
[141]
[116]
[
150
]
[83]
[
151
]
[
152
]
[108]
[
153
]
MCP-1 (CCL2)
[118]
[112]
[
154
]
[
155
]
[147]
[149]
[
156
]
[116]
[40]
MIP-1 (CCL3)
[108]
[147]
[
157
]
[153]
MIP-1 (CCL4)
[153
[147]
[112]
[83]
[
158
]
RANTES (CCL5)
[147]
[112]
[149]
[
159
]
Fractalkine
(CX3CL1)
[159]
Table 10.2 is an overview of studies providing evidence for the production and function of chemokines in patients with
severe TBI or experimental animal models of head injury. Note that studies investigating IL-8 in rodents predominantly
focus on MIP-2 (CXCL2) and KC (CXCL1), which are considered the functional homologues of human IL-8 (CXCL8).
Listed in parentheses beside each traditional chemokine name is the systematic nomenclature.
