CCL2 modulates cytokine production in cultured mouse astrocytes

Research output: Contribution to journalArticleResearchpeer-review

40 Citations (Scopus)

Abstract

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.
Original languageEnglish
Pages (from-to)1 - 11
Number of pages11
JournalJournal of Neuroinflammation
Volume7
Issue number67
DOIs
Publication statusPublished - 2010

Cite this

@article{82f87176ec2348e5a5780b228e37faeb,
title = "CCL2 modulates cytokine production in cultured mouse astrocytes",
abstract = "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.",
author = "Bridgette Semple and Frugier, {Tony J} and Morganti-Kossmann, {Maria Cristina}",
year = "2010",
doi = "10.1186/1742-2094-7-67",
language = "English",
volume = "7",
pages = "1 -- 11",
journal = "Journal of Neuroinflammation",
issn = "1742-2094",
publisher = "Springer-Verlag London Ltd.",
number = "67",

}

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 journalArticleResearchpeer-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 -