Abstract
| Original language | English |
|---|---|
| Pages (from-to) | 1 - 11 |
| Number of pages | 11 |
| Journal | Journal of Neuroinflammation |
| Volume | 7 |
| Issue number | 67 |
| DOIs | |
| Publication status | Published - 2010 |
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CCL2 modulates cytokine production in cultured mouse astrocytes. / Semple, Bridgette; Frugier, Tony J; Morganti-Kossmann, Maria Cristina.
In: Journal of Neuroinflammation, Vol. 7, No. 67, 2010, p. 1 - 11.Research output: Contribution to journal › Article › Research › peer-review
TY - JOUR
T1 - CCL2 modulates cytokine production in cultured mouse astrocytes
AU - Semple, Bridgette
AU - Frugier, Tony J
AU - Morganti-Kossmann, Maria Cristina
PY - 2010
Y1 - 2010
N2 - The chemokine CCL2 (also known as monocyte chemoattractant protein-1, or MCP-1) is upregulated in patients and rodent models of traumatic brain injury (TBI), contributing to post-traumatic neuroinflammation and degeneration by directing the infiltration of blood-derived macrophages into the injured brain. Our laboratory has previously reported that Ccl2-/- mice show reduced macrophage accumulation and tissue damage, corresponding to improved motor recovery, following experimental TBI. Surprisingly, Ccl2-deficient mice also exhibited delayed but exacerbated secretion of key proinflammatory cytokines in the injured cortex. Thus we sought to further characterise CCL2 s potential ability to modulate immunoactivation of astrocytes in vitro.
AB - The chemokine CCL2 (also known as monocyte chemoattractant protein-1, or MCP-1) is upregulated in patients and rodent models of traumatic brain injury (TBI), contributing to post-traumatic neuroinflammation and degeneration by directing the infiltration of blood-derived macrophages into the injured brain. Our laboratory has previously reported that Ccl2-/- mice show reduced macrophage accumulation and tissue damage, corresponding to improved motor recovery, following experimental TBI. Surprisingly, Ccl2-deficient mice also exhibited delayed but exacerbated secretion of key proinflammatory cytokines in the injured cortex. Thus we sought to further characterise CCL2 s potential ability to modulate immunoactivation of astrocytes in vitro.
UR - http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2964657/pdf/1742-2094-7-67.pdf
U2 - 10.1186/1742-2094-7-67
DO - 10.1186/1742-2094-7-67
M3 - Article
VL - 7
SP - 1
EP - 11
JO - Journal of Neuroinflammation
JF - Journal of Neuroinflammation
SN - 1742-2094
IS - 67
ER -